Alrighty, let's go ahead and get started. Welcome, everyone, to the 44th Annual J.P. Morgan Healthcare Conference. My name's Anupam Rama. I am one of the Senior Biotech Analysts here at J.P. Morgan. I'm joined by my squad, Ratih Phinney, Priyanka Grover, and Joyce Zhao. Yeah, I almost called her Jay-Z. That's what I normally do. Our next presenting company is Neurocrine, and presenting on behalf of the company, we have Kyle Gano, CEO.
Thanks, Anupam, and thanks to the J.P. Morgan squad and J.P. Morgan for having Neurocrine here at the end of the first day. Really is a great way to kick off the week and year for the company. So maybe just to kick things off here, some housekeeping. I will be making forward-looking statements and like to direct you all to our latest SEC filings for the risk factors of the business. With that behind us, then I really would like to ground everyone here in two overarching themes that are important for Neurocrine for 2026. One here, as you can see from the slides, strong and building momentum, and the other, strategic balanced diversification. So I would like to touch on these in the first slide and then pull these themes through as I go through the presentation this morning.
Just to kick off on momentum, what I'm talking about here, I'm sure you all took physics back in college, the literal physics definition of momentum, mass times velocity. I like equations. I use them a lot when I speak. I think for today it's a good example for me to lean on. For Neurocrine, we have more mass, more velocity than ever before. With 2,000 people at the company, we have a proven track record of discovering, developing, and commercializing medicines for patients. In fact, you can see from the slide, we have four FDA-approved medicines on the market. All these were first in class at the time of their approval. We commercialize INGREZZA and CRENESSITY here in the U.S. ourselves. Now, this slide here has a lot of information, so I'm going to just touch on a few things on INGREZZA and CRENESSITY . We're still in 2025.
We haven't reported Q4, so I'm giving you some 2025 insights into the business. In 2025, we guided INGREZZA to $2.5 billion-$2.55 billion in net sales. For CRENESSITY, our first full year of commercialization of the medicine, I'm reporting the first nine months, $166 million in net sales. A great kickoff, great start to CRENESSITY. Now, on INGREZZA, we built it into a blockbuster franchise. We've got multiple dosage strengths formulations. For CRENESSITY, we see a line of sight with it being our next blockbuster in a rare endocrine disease called classic congenital adrenal hyperplasia. Building things takes execution, and we have a lot of that going on at the company right now, not just in day-to-day activities, but for both of these brands, we're actually undergoing a sales force expansion currently.
We can talk more about that when we break out to our Q&A here at the end or during the week, but a lot of execution going on on the commercial side of the business, and likewise, we're executing on a leading neuropsychiatry portfolio, which we believe is poised to bring to patients multiple first and best class medicines this decade, so a lot of momentum, a lot of execution in 2026. What about diversification? Until a few years ago, Neurocrine was a single product company. This is with INGREZZA, and we were singularly focused on small molecules. That's not the case anymore. We are scaled. I mentioned the employee base that we have, and we are a diversified biopharmaceutical company now. CRENESSITY plays a big role in that.
You can see from the slide here, sales and revenue are coming from another product for the first time since INGREZZA's approval in 2017. These two products will work together to grow revenue over time as well as revenue diversification, which is an important goal for the company. Likewise, we see the opportunity to provide continued durable cash flows, and both medicines will allow us to have a very solid foundation from which to invest in R&D over the long term. So that's the commercial side of the diversification. What about R&D? Well, we're using our Transform R&D Engine, which I'll talk a little bit about today. It's fully operational. It's delivering. It's performing. We're leaning on that as well as 30 years in CRF biology. CRF is corticotropin-releasing factor, and we're diversifying into new therapeutic areas.
When we have as much biology but much experience as we do, moving into new modality in this space or new disease state is very efficient. So we like what we're doing here with our engine in R&D as well as in CRF. Now, in terms of our pipeline, we also see strategic diversification as well. I mentioned the small molecule focus historically. We're moving into new modalities, peptides, antibodies, gene therapies, and these are all anchored around this mindset that we have, a philosophy, if you will, of matching the right modality with the right target in a given disease. And likewise, when we think about these modalities, they're going to offer us the opportunity to improve probability of success ultimately as we move these through clinical development. It's done with a discipline mix for the first time of internal innovation.
We're doing more internally, and of course, we're always going to lean on strategic business development to help accelerate what we would like to do in the pipeline. So if you think about what we've done here, there's a lot of growth in the company the past seven to 10 years, and we're not growing for growth's sake. It's been strategic. It's been deliberate. It allows us to minimize, helps us improve our probability of success across the portfolio, helps us be more resilient in the long term. And by looking at those different pieces, it also allows us to focus on our areas that we have the most expertise. So if you think about this, our overarching themes that I've shared, you can understand why we believe we're entering one of the most exciting opportunity times and moments here at Neurocrine in our history.
So that's what I'm going to try to share and impart with you today and what we're planning for 2026 and beyond. So the heart and soul of the company is our R&D Engine. It was this time last year that I presented what we're trying to achieve in an R&D transformation. It was last month that I told you that our R&D Engine is fully operational. I think this slide goes a long way at making that transformation tangible. I just mentioned a moment ago what the goal is here. The idea is from a philosophy perspective to remain disciplined and always match the right modality to a given target in a disease of interest. And that's exactly what we've been able to do and focus on the past several years. And that discipline has given us an increase in our productivity.
What we're looking at from a year-to-year basis at steady state, targeting four new phase I programs, advancing two new phase II programs, and have a sustained phase III portfolio of at least three programs. We believe if we continue doing this level of output year after year, we'll be able to meet our objective of one new medicine every two years. That's the plan. It's going to take a few years for us to move all of our early clinical entrants from phase I to phase II and phase III. That's why we believe we'll be at steady state by the end of this decade. Now, this model isn't theoretical. We have achieved for the first time our phase I through phase III metrics in 2025.
As you'll see as we go through our pipeline for this year, we're well on our way of doing it again. Building on the momentum of our R&D Engine is our neuropsychiatry portfolio. There's a lot going on across the pipeline in this area. It's an area of key expertise and strength for the company. It also represents long-term value creation for us when you think about what's going on in early stage development all the way to phase III. The main point that I'd like to leave with you all here today is that psychiatry neurology is inherently risky. We anchor all of our programs, all of our targets around validated biology. It doesn't give you certainty with success, but it does help your odds.
When we think about our first-in-class AMPA- PAM, this is one of the most compelling programs in the area of major depressive disorder today, but it leans on validated biology within the glutamate system, which was validated by ketamine and other psychedelics over the past many decades. We're really excited about this program, spectacular phase II results, clinically meaningful, statistically significant, very good safety and tolerability. It's why we pushed this program into phase III as quickly as we could in order to get this medicine to patients. Now, Derecladine, we could say the same thing. It's our selective muscarinic M4 agonist, again, for schizophrenia, as you know. It's in all of its phase III trials currently, and we started a phase II trial in bipolar mania towards the end of last year.
Both Osovampator and Derecladine, in my opinion, if you look at them together, represent medicines that can really change the standard of care for patients. And if you look at their biology, it intersects so many different disease states. I mentioned two for Derecladine. It gives us the opportunity for many chances for long-term value creation as we pursue other indications. Now, you can see from this slide, there's a lot of breadth and depth to the muscarinic portfolio. We have agonist. We have antagonist. We have molecules in different disease states. We have them in different stages. Again, very deliberate and intentional how we put this together. Given the multitude of the programs, it gives us the opportunity to tackle many different patient populations.
That increases the probability of success, and it gives us the opportunity to really play in some of the largest disease states and markets in the world today. So we would like what's happening there with the muscarinic portfolio. On the VMAT2 side of the pipeline, you can see that we're advancing two new next-generation VMAT2 inhibitors. The sole purpose here is to extend our leadership position in VMAT2 biology that was set by INGREZZA 20 years ago. We have two molecules in development, NBI- 890 and NBI-675. These were internally discovered molecules with physicochemical properties that are distinct from INGREZZA. And we believe this will give us the opportunity to reach many more patients. So if you look at INGREZZA, you look at NBI-890 and NBI-675, this is a category that's built for the long run and can allow us to continue to have this leadership position.
Building on the momentum of our neuropsychiatry portfolio is our emerging endocrinology pipeline. And today, endocrinology is CRF. Everything goes through CRF in the company right now, whether you're talking about our two-pronged strategy, which comprises CRF1 tackling HPA axis to dysregulated diseases, or if you're looking at CRF2 in metabolic diseases and disorders. Again, this is the power of working in a space for 30 years. This also gives you the ability to strategically diversify, whether you're talking about moving a small molecule program like CRENESSITY into a peptide for the same disease state, very incremental diversification required for there, or you're taking a CRF1 mechanism and moving to CRF2 in metabolic disorders. These are all things that are common and familiar to us.
What I'd like to walk you through is a little bit about the strategy, and that will set the stage for the remainder of the presentation. On the left here, you can see that the foundation is being set by CRENESSITY, our medicine for classic congenital adrenal hyperplasia. We have a next-generation peptide moving through development. That's NBI-P-1435. I'll share with you some data on that shortly. That's going to be a first-in-class subcutaneous injectable for patients with CAH, giving them greater flexibility, as you'll see from the PK profile, perhaps even enhanced efficacy. Beyond that, we'll be introducing a new molecule to clinical development later this year, NBI-1A8, that will lean into the same pathway, but for a women's health disease. So stay tuned on that. We'll share more when that starts clinical development. Now, on the other side of our strategy is CRF2.
This allows us to extend our leadership position set by CRENESSITY into a related area of biology. But our first program in this space is centered in obesity. Our first molecule here is NBI-P-2118. It's set to be a once-weekly injectable for patients that are obese or for obesity as an indication, with a clear product profile that differentiates it from current standard of care. Namely, we're looking at comparable levels of efficacy as incretins or better, improved GI tolerability, a very simplified titration schedule, or the absence of the need of titration. When we think about obesity, what we're also targeting is quality weight loss. So we're looking at weight loss targeting fat versus lean mass. So muscle mass preservation is a key cornerstone of what we'd like to do on this right-hand side of our two-pronged strategy in CRF.
Now, by quality weight loss, we understand, and we've seen out there in the news how the loss of lean mass can decrease metabolic outcomes. We also see that as a key driver of long-term tolerability concerns with some of the GLPs and other incretins that are on the market. We're tackling all these with one singular mechanism, CRF2. So we believe we have a very differentiated approach in an area that we believe we have deep institutional knowledge in. Now, we're not just done with 2118. This is a must-win category. We're moving these programs quickly through clinical development. We also have a combination approach. So we've developed our own proprietary incretin in-house. It's a triple G. You can see some of the details here of how we characterized it. We're doing a mix-and-match strategy with 2118, and we've also conjugated it directly to 2018 as a standalone treatment.
This approach offers all the benefits of the 2118 program exactly, but potentially greater weight loss than the single agent itself. So we're excited to offer that to patients moving forward. And then lastly, I'll call out here, moving through late-stage preclinical development, is our own long-acting proprietary triple G that's been conjugated to an Fc portion of an antibody, giving us a differentiated approach still, and that can be combined with NBI-P-2118. So a very rich endocrinology pipeline, and I would say it's a very rich CRF pipeline. Both of these are used interchangeably at Neurocrine and rely on a lot of history that we've developed here at the company. So with that kind of setting the stage, I'd like to go back to where it all started, and that's with CRENESSITY.
We have some new data, in particular two-year results related to our open-label extension from the CAHtalyst studies, which we branded for the adult and pediatric double-blind placebo trials that were used for approval. I'm going to share some highlights here with you today. Just appreciate this is hot-off-the-press data. We have a lot of data sets that are currently being reviewed, and we're preparing abstracts and presentation posters that will be made available to you all at upcoming endocrinology meetings this spring and certainly by endo in June. So I've got three different areas that I'm going to touch on. I'm going to summarize at a high level what we've seen across the adult and pediatric studies. That's going to be done here. I'll give you a little bit of data from the adult OLE or open-label extension. I'll share some data in the pediatric patient population.
There is a breadth of information that is incredible coming out of this open-label extension work that we've done. There's a lot of depth that's there that's going to be coming out over the next couple of months. I can't get through all of that here. I'm going to give you little flavors of it so you can get a feel for what's coming your way. So when we think about the adults and pediatrics, what we can say is after two years of treatment with CRENESSITY, very robust, sustained clinically meaningful benefits over that entire period of time. These are the type of outcomes that you want to see in a real-world setting. If you drill down a little bit more, what I'm talking about here is CRENESSITY enables the reduction of androgens and ACTH and maintains them at that level through the course of treatment.
CRENESSITY enables steroid reduction and to levels that bring a very high percentage of patients into that physiological range. At the same time, these same patients have their androgens maintained at baseline levels. So very robust, durable efficacy results there. On safety and tolerability at two years, CRENESSITY continues to be very, very well tolerated. We have an 80% retention rate across this two-year time point. No new safety warnings or safety issue signals. But most importantly, now we've accumulated 35,000 patient weeks of exposure. Very good safety, very good tolerability across the board. So if you put these two together, you understand why CRENESSITY is an anchor of our endocrinology pipeline and anchor of what we want to do in CRF. Now, let's drill down and talk a little bit about the CAH adult study quickly.
Here we're able to show that about 70% of patients were taken to the physiological range of 11 mg/ m squared per day. That's a threshold that was agreed upon by us with the FDA for our pivotal studies. At the same time, these same patients that came into the study were able to show that their androgen levels were maintained at baseline levels. So a very good one-two punch there coming out of this open-label extension data at month 12, 18, and 24 over the entire treatment period. Now, I should have mentioned at the introduction of this slide that the key objective for adults with CAH is to reduce excessive exposure to steroids and therefore minimize cardiometabolic comorbidities like obesity and insulin resistance. So we see this great data on moving patients into the physiological range, but how does that transform the trajectory of their cardiometabolic parameters?
And what I have to share with you here today is on the obesity side of things, since that's a theme here. Patients coming into the double-blind placebo-controlled portion, about 80% of those patients were obese or overweight. During this two-year period, about 40% of those went on to see a 5% or greater weight loss. It's a very impressive data set there. When you line the efficacy with this change in cardiometabolic trajectory, you can see that the objectives were exactly met here in this open-label extension in terms of what adults with CAH patients are looking for. So very strong data there in the adult side of the equation. What about pediatrics? Pediatrics are a patient population in CAH that presents their own clinical context that's distinct from adults.
There's a range of symptoms and a range of treatment goals that these patients aspire for over the course of their maturation. Depending on age, they could be very much focused on avoiding adrenal crisis, or they could be looking at ways that they can maximize their potential height. These are all these things that we keep in mind when we think about studies in the pediatric patient population. But for us, it all starts with ACTH. And then we talk a lot about androstenedione. The ACTH is a very critical hormone, especially in the maturing child as they go from adolescence to teenage and ultimately adult years. So why is ACTH so important? Well, in CAH, as you can recall from my prior slides, it's a disease of HPA axis dysregulation. And what this translates to is ACTH overproduction.
Looking at ACTH has a very important role for us because we can look at target engagement and understand that we're making a difference in the underlying disease if we can remove or reduce excess of ACTH. You can see that from looking at the 12, 18, and 24 months data. We can do that exactly with CRENESSITY. The other thing that I'd point out about ACTH is that normal ACTH functioning is critical for normal physiological functioning. The body has compensatory mechanisms to fight things like adrenal insufficiency to help the body grow and have normal development. Having normal ACTH signaling is critical in that process. The last thing I will say, and it's related to my previous message, is that ACTH as a hormone activates multiple receptor types. I know on the adrenal gland, the HPA axis components of CAH, we often refer to melanocortin-2.
ACTH activates melanocortin-1, melanocortin-3, melanocortin-4, and melanocortin-5. You don't want to be overactivating the receptors continuously during the course of a child's life. That's exactly what's happening today in a CAH patient that's not on CRENESSITY or in a CAH patient that may receive a different approach that's in development now or in the future. We believe our approach is very differentiating and being able to reduce this excess of ACTH in patients and maintain them at a level that allows for normal ACTH signaling. A related point to that, just to wrap up this slide, CRENESSITY does not bind to or affect vasopressin-induced ACTH release. It's a very important distinction because when patients use CRENESSITY, they're allowed to have the normal ACTH-mediated stress response. That, in turn, is one of those mechanisms that the body uses to fight or resist adrenal crises, adrenal insufficiency.
In our trials, we saw very low rates of adrenal insufficiency. In fact, in the pediatric double-blind portion of this catalyst program, we saw zero. In the adult study, we saw a very low rate of 1.6%, and the active and placebo were exactly the same. Taken together with CRENESSITY, we can show that we can enable ACTH dose reduction or ACTH excess reduction and maintain them at this level. We can also affect the underlying biology of the disease. Now, I mentioned on the prior slide that one of the important treatment goals for patients is to maximize patient height. Now, while our catalyst study wasn't designed to do so, in fact, most of the patients coming into the double-blind portion of the pediatric trial were pubertal and were not able to really see much significant growth during the course of the study.
There was a subset that was. They were pre-pubertal, and they did have the opportunity to grow, especially in a long-term open-label extension like this for a two-year period. We have some data coming through on those subjects, and in the subset that we've analyzed, we've shown that we were able to slow the bone age advancement in these patients. In fact, if you look at their data a little bit more closely, we predict that their adult height will increase by roughly five and a half centimeters or over two inches. This is a very clinically meaningful result in a study of this size, especially since we weren't looking to achieve this at the outset in terms of a primary or secondary endpoint. So very robust results. Let me just put a pin in it because oftentimes a picture says a thousand words.
In a pediatric CAH patient, their bone age advances more quickly than their chronological age, and the way that physicians often view this is looking at their growth chart curves, for example, on the right. Y-axis height, X-axis here, bone age and chronological age. In an ideal world, in a patient without CAH, their bone age and chronological age track each other, and the red circles and the green triangles are right on top of each other. You can see here when a subject, in this case, an eight-year-old, entered this open-label extension, their chronological age was separated significantly from their bone age from eight versus 13 and a half years. When they started CRENESSITY, we were essentially arresting their bone age advancement, and over this two-year period, you see a collapsing between the bone age and chronological age. This is exactly what you want to see.
It maximizes the time this patient is able to grow. So this is something we'll be teasing out a lot more as we get into the data set, but very compelling, very broad data sets coming out of this OLE. Now, CRENESSITY sets the foundation, but we're hardly done yet. We want to be a leader in this field. That's why we have a next generation of medicine in phase I development. I'm sharing you all here today data for the first time. Some of the interesting aspects of it, we've looked at four different cohorts in our phase I study. So far, it's been safe and well tolerated. We see a half-life of about 10 days. This supports infrequent dosing. In fact, we're believing that this is going to be one week or better subcutaneous injection for patients.
The next steps and quickly on this is that obviously we know the pathway to approval that's been set by CRENESSITY. We'll be following a similar path. Right now, we're looking at finding the right dose or doses to take into mid- to late-stage development, and we're able to do that through a mature bone challenge test to determine the PD effect following ACTH stimulation. This part of the phase I program is ongoing now. We'll look at starting phase II, III later this year, so that's MPI P1435. Now, if we look at all the slides I've shared, we've done a lot today. I've shared with you about the science, the data, the CRF platform. How does this all pull together? Well, we've got 12 programs in clinical development today. Eight in phase I, two in phase II, and another two in phase III.
They've been developed and put into these stages deliberately, intentionally. They're all founded in our areas of strength: neurology, psychiatry, endocrinology, and all attached to validated biology. Those are things that we like. From a modality perspective, you see expansion into peptides and biologics and even gene therapies. We see some of the studies that will be initiated this year. Again, all founded on the premise of matching the right modality with the right target. So we've got late-stage opportunities, mid-stage opportunities, and future opportunities for growth with phase I programs. We're not trying to initiate studies for initiating studies' sake. They're all built around a robust R&D engine, pipeline prioritization, and making sure that we convert all of our science into clinical execution. So quickly, we've got six programs that we're planning on initiating in phase I this year.
Our Friedreich's ataxia program for gene therapy will enter in the second half. We've mentioned our two obesity programs. Those are starting this year as well. Our other program in HPA axis dysregulation and other CRF antagonists will be starting, and two new immunology programs, so a lot going on at Neurocrine, and to deliver that pipeline is a lot of execution. I've touched on that already. I think I'll leave some of those topics for Q&A. In terms of new study initiations, excuse me, what we've got, in addition to the six new phase Is, our new phase II trials to help round out some of the work with CRENESSITY as well as moving forward our next generation VMAT2 inhibitor, 567, and an Alzheimer's trial, and of course, our next generation medicine for CRENESSITY. A lot going on there.
These do meet our R&D objectives for the year. In fact, we're exceeding the targets that I mentioned early on, which is a good thing. That means we're accelerating us down that path for reaching steady state. So all this execution leads to momentum in 2027. It's all about getting to our phase III readouts for Osovampator and Derecladine. Again, these are medicines that will change the standard of care across both MDD and schizophrenia. With that data being positive, NDA submissions follow, and then commercializations shortly thereafter. The sales force expansion that we're rolling out for INGREZZA will be quite nice for the receiving of these medicines once they're available later this decade. phase I data we're looking for in 2027 pertains to our gene therapy program and Friedreich's ataxia.
We also have and anticipate weight loss data from our first CRF2 peptide in some of our early phase I studies. And then in phase I, we expect safety and biomarker data coming out of our muscarinic program and our early immunology program. So a lot of data flow, a lot of data coming out over the next couple of years, starting with 2027 and then a regular flow from thereafter. I will mention. I should have said on the previous slide, we will be having a Neurocrine webinar day later this year to go over some of the early neurology and immunology assets that are not characterized here today. So I think with that, I'd like to jump into Q&A. Why don't we have our team come up and we could take your questions. But thank you very much for hearing me out today.
Look forward to meeting with you all this week.
Kyle, you want to just quickly introduce everybody that's on stage?
Yeah. So quick introduction here as folks come up. Sanjay Keswani here at the end is our new Chief Medical Officer. He joined in June. So anything R&D in the pipeline, please ask him. I know he's anxious to answer many of your questions.
Jude Onyia is our Chief Scientific Officer. He joined the company in November of 2021. He's really the engineer behind our R&D engine that I described early on. Eric Benevich is here as well, our Chief Commercial Officer. I know you very well. You know very well. Samir Siddhanti is our head of business development and strategy. And of course, Matt Abernethy, our CFO.
Kyle, I was wondering if you could put into context what you're seeing in the first year of launch for CRENESSITY and how does it compare to some of your analogs or internal expectations?
Since I've been talking for 25 minutes and we have our Chief Commercial Officer here, Eric, you want to give your thoughts?
Yeah. In a word, it's beat our expectations. Just to level set everyone, classic CAH. CRENESSITY is the first approved treatment. These patients have been living with a standard of care of super physiologic glucocorticoids for over seven decades. Going into the launch, we're just past one year of the approval of CRENESSITY. You may recall it got approved in mid-December of 2024. Certainly, in some ways, there are some aspects of this launch that are similar to what we experience with INGREZZA and tardive dyskinesia. It's a first in class and a first in disease medicine. We've characterized this as a learning launch. What I would say is that we've learned a lot over the first year. There's three areas that I think have been favorable versus our expectation. The first is really the receptivity from the patient and endocrinology communities.
The uptake has been faster than what we expected coming out of the gate, really since the very beginning. And the adoption rate has been very steady and consistent. And I should characterize my comments as really for the first three quarters of 2025. We're not making any interquarter commentary here, but very consistent in terms of the rate of adoption from week to week and from month to month. The second thing that's been really favorable versus our expectations has been the reimbursement. So we expected as a new medicine without any formulary coverage that most of these patients would require a month or possibly two of free goods before getting reimbursement from their insurance company. And what we found really since the very beginning is that most of these patients were able to get commercially reimbursed coverage within a week. And so reimbursement has been very favorable.
Then the third thing that's been favorable from our perspective has been the persistence. Kyle talked about that with regards to the two-year open-label extension. Certainly, we saw very strong persistence in the double-blind studies as well. Over 90% of patients in the adult and pediatric studies completed and rolled over into the open-label extension. As Kyle said, over 80% have completed through two years in that open-label study. Our real-world experience has been that these patients get started on treatment and they tend to stay on treatment. Between the very steady and consistent rate of adoption and then patients staying on therapy, we've really seen a nice growth curve in terms of our ability to really help that patient population. Overall, we're really pleased with the first year that we recognize that we've got a long way to go.
There's approximately 20,000 or so classic CAH patients in the U.S. as we estimate. And we've made a penetration of roughly 10% of that in the first year. And so we're looking forward to helping many more patients with classic CAH in 2026 and beyond.
Kyle, you presented some new two-year CAH data just today, hot off the press. I was wondering, Eric, if I could have you expand on your comments just now about how these types of data could help you commercially as you're going into the second year and launch year.
Sure. If you think about what's going to allow us to continue to develop the CAH opportunity to help more patients, there's a couple of things. One, and Kyle touched on this, the really favorable safety profile. We've got very good labeling, and we also have very good long-term safety with over 35,000 patient weeks of exposure to date. I think that's very reassuring for endocrinologists and for patients when they're contemplating initiating treatment. So that's one thing. The second thing, and Kyle mentioned this earlier, is that we are expanding our CRENESSITY sales team. And really, I would characterize that as building on momentum and building on growth.
The reason that we're doing it, and I mentioned this last night at our dinner, had we known some of the things that we've learned in the first year of the launch, we probably would have launched with a larger sales team. And so ultimately, this gives us the ability to go deeper within the endocrinology audience and also to start to tap into some of the patients that are not currently under the care of an endocrinologist, for example, that are being cared for in a primary care practice or an OB-GYN practice. So I think those are going to be some of the drivers of growth. And then, of course, the continued strong reimbursement that we've been seeing really since the very beginning of the launch.
Sanjay, do you want to comment on the data?
Yeah, I think Eric made some really important points there. The long-term safety and tolerability we have in patients with CAH is really outstanding. We're very happy about that, and that's particularly important for physicians and parents of patients who are often young children because this is a medication they'll be taking potentially for many, many years. The other thing is that we've seen the long-term consequences of steroid reduction, as people in this room are aware. Chronic steroid use is associated with weight gain, glucose abnormalities, including type 2 diabetes, bone issues, including osteoporosis, and we've seen some really encouraging data with respect to weight loss, improved insulin resistance, and also advancement or attenuation of advancement of bone age, which is incredibly important, particularly as children are growing. You ideally want them to achieve their full potential with respect to adult height.
And essentially, the earlier we intervene, the better. And that's what we're seeing in our studies. So really very excited and encouraged by the data we're seeing.
As a parent of a CAH patient, I think many of you guys know that my son was the first patient on CRENESSITY, which is quite a blessing to be part of a company like this. And looking at that bone age curve, I think I said this to Priyanka, that's golden. If you're a parent walking into a clinician's office with an eight-year-old with a 13- or 14-year-old bone age, that doesn't feel very good. But two years into taking CRENESSITY to see that bone age to chronological age, the age gap shrink like that by two years, that's quite remarkable. So it is encouraging to see these data. And I can speak as a parent to both see the efficacy there as well as the safety, just quite phenomenal.
Kudos to Eiry, who's not here for the first time and helping develop the medicine, and everybody who's been a part of the launch. It's been quite rewarding.
Matt, thank you for sharing that. And I think that's a great place to end. Thank you so much.