Biomarin Pharmaceutical Inc (BMRN) September 10, 2026 Conference Transcript

All right, everyone. Well, welcome to day two of Citi's Back to School Biopharma Conference. I'm Eric Joseph, Senior Biotech Analyst with the firm, and this session is with Biomarin, and I'm happy to be joined by Chief R&D Officer Greg Freeberg and Chief Commercial Officer Kristen Hubbards. Thank you both for joining us here. Maybe just before we kind of dig into questions, it would be good to kind of have some high-level remarks from you both and just what some of the key priorities are at the company, you know, looking over the next six, 12 months.

And thank you so much for having us, Eric. So just to take a step back, Biomarin, we're a leading global rare disease company, and we're really focused in and around genetically defined conditions. And what we have now is nine commercial therapies across how we're organized, which is in two business units. And that includes skeletal conditions and metabolic conditions. Now we're a highly profitable company. We have strong revenue growth and really we're increasing cash flow, which is fueled in large part by the patient demand that we are creating across the 80 country footprint that we work in. Now, we recently in our Q2 call announced that we've got four products that are tracking to blockbuster status, which we're excited about. And Voxogo is in the lead. So at our full year 2026 guide, we had said that Voxogo, the range would be 1 billion to 1.05 billion. So that'll be our first Blockbuster product this year. And what also happened this year that we talked quite a bit about in the Q2 call was the closing of the Amicus acquisition. So what that did for us was it brought in two high growth commercial products that is Gallifold for Febre and Pombility and Opfolda, which we call POMOP for Pompe disease. And what we shared in the call was that our peak potential for Gallifold is at $1.4 billion in the mid-2030s. And for Pombility and Upfolda, that's $1.2 billion potential in the mid to late 2030s. So as a company, we really do, or after this acquisition, we really do expect substantial non-GAAP EPS accretion from these assets in 2027. And we really are generating significant cash flow from it that we can then reinvest in innovation. So with that, I'll hand it over to you, Greg.

Thank you, Kristen. Everyone can hear me okay? Thank you for the invite. It's fantastic to be able to talk a bit about Biomarin's research and development. We are in the process of building out our pipeline, but there are a couple of highlights I want to share for you. One is actually published just yesterday, so hot off the press, our hypochondroplasia data. So this is taking the CNP analog Voxogo and applying it to a related but distinct disease hypochondroplasia. Those results actually exceeded our expectations, both from a growth standpoint, as well as some of the secondary endpoints. We're very proud of that data. It's actually been submitted to the FDA, and we'll be able to update folks soon once that filing is accepted and we have a PDUFA date. If you think back more towards the pipeline, we've had two new additions to the pipeline, and one that came along with the amicus acquisition molecule that was referred to as DMX200 from dimerics. We have the U.S. rights. We call it BMN820. This is for focal segmental glomerulus sclerosis, so FSGS. It's a CCR2 oral inhibitor, and that is a phase three program running in that renal indication, which will have phase three data looking at two-year proteinuria out in uh, 2028. So thrilled to be able to add that in the U S rights to that molecule. And, uh, another hot off the press, uh, uh, update for you. We closed just last week, uh, acquisition of a post phase one product from Alesta therapeutics. This is a L E O one. This is a molecule that's, uh, uh, trying to, um, uh, address, uh, hypophosphatasia, but rather than being an enzyme replacement, this is more of a substrate reduction therapy. Again, the promise there is that not only might you have an oral convenient therapy, but there may be an opportunity to reach some of the tissues that the bone targeting biologics are unable to reach just because of their PK and their distribution. That includes muscle and joint and so forth. I'll just wrap up by saying that we've got internal innovation as well that's continuing to percolate through our pipeline. Probably the star of the show is BMN 333, which is our next generation cnp analog more long-acting weekly administration and our goal there i think we'll talk about it a little bit more is going to be to actually deliver a greater pharmacodynamic effect than what voxogo can achieve and we have a variety of proof points again that tell us that we're headed in the right direction and we have a molecule that can answer this question definitively that's in phase two right now we're enrolling and it will have data available next year before we launch a seamless phase three thereafter.

Okay. Well, great. Yeah. Lots to dig in there. I think it might bring us all the way back to the start with Voxogo and the commercial franchise and a contraplasia today. I guess one of the things that's come across in the, for a couple quarter updates now is just the growth that you're seeing within the under age two cohort of the market, Right. Can you just talk about sort of how much headroom that segment happened, how much headroom for further penetration you're seeing in the under two year old population and how much of a growth driver this could be going forward? And then perhaps even just stepping back as we think about the franchise as a whole within a contraplasia, what some of the key growth opportunities are looking forward?

Yeah, thank you for the question. So specifically to Vox Ogo, we did report in our earnings call strong growth. So revenue at 14% year over year, and importantly, patient demand at 20% year over year. And that's our global numbers. And what we had said is that in particular, that growth, and especially in the US is being driven by exactly what you just referenced, Eric, and that is that zero to two population. It is such an important population for this therapy, most importantly, because if you look at medical consensus guidelines, it really does suggest that you treat right at the time of diagnosis, because that is where that child can then, you know, benefit the most in the long run. And so we're really excited that we have the exclusive label there, and we anticipate being the only product approved in the zero to two population for the next couple of years. And so that's an area that we really do see exciting growth coming out of. Not to mention some of the other growth drivers are that we're continuing to expand and accelerate in certain countries globally outside the U.S. So as a reminder, 75% of our revenues come from outside the U.S. And there we have growth happening in countries where we're already well-established. And this is where you see the highest growth coming from that zero to two population because it's an incident population that you're catching at birth. In other countries, we're either newly launching or still expanding into those countries, and so you see growth across all age groups. So it really does come down to a kind of country-by-country look at where that growth is coming from. But in total, we are commercialized in 55 markets in our 80-country footprint, and that is an area that we'll continue to grow in. So very exciting for achondroplasia, and I certainly want to mention the fact that what we also announced since the quarter closed was the settlement that we reached with Ascendis in terms of getting royalties on net sales of UVAwell, which was the first competitor to launch in this space. So we have a 20% royalty on U.S. net sales and an 18% royalty in the EU, Brazil, and South Korea. And what excites us most about this is that this does just kind of clear an overhang for us. This is something that enables us to capture value right away, which our ITC proceedings would not have done. we would have been in further litigation in both the U.S. courts as well as the jurisdictions where our IP is. But I think most importantly for us, we think that this is a really important moment for both patients as well as Biomarin to kind of clear this overhang and be able to move forward. So that's looking at achondroplasia. But another big and exciting growth driver for VoxSogo is in hypochondroplasia. And I know you'll speak more to this, but we're anticipating a launch should the regulatory bodies approve in the coming year so we have the team certainly gearing up around that and then as we look further out we are looking to as as greg had mentioned really bring forward the um you know hopefully best in class long-acting cnp so the durability of that franchise you can see over time growing um let's hold off on hypochondroplasia uh for a second can just kind of stick with achondroplasia.

So two things. One, just, you know, picking up on the competitive dynamic a little bit with you well now, right? Appreciating that, you know, the settlement does allow you to capture, you know, some preserve, I guess, value, right? Or capture some upside, I guess, of the front versus ongoing litigation.

I guess that said, from a share standpoint um what do you anticipate in terms of switching away to you well uh from the existing franchise and then um yeah i'll leave the question there and follow up on a different uh different point in a second so so what we shared excuse me so far has been that we've seen 90 retention on voxogo out through july so mind you that uva well launched in february we've still 10% have now switched in the U.S., which is where they've launched. 10% have switched over to UVOL. We've retained 90% on Voxogo. And primarily what we hear from families around why they've stayed is multifold. One is that they're seeing the benefit of the product, and that for them is really important when they know that the safety is there, the efficacy is there, and they're seeing their child benefit from it. In addition to that, many have created a daily routine that they're comfortable with and that that's working for them. And then we've also heard that they've really appreciated the wraparound services that we have put in place with our clinical coordinator team who are there to help them with injection education, et cetera. That has been beneficial. So that is in large part what we've heard. What that story turns out to be, we are monitoring very closely. We will continue to provide color on as we see more, but we're quite happy with seeing that 90% have stayed. And I think it also does show that achondroplasia, in particular in the U.S., is not an easy market just to come into and just kind of overturn or somehow capture all the market share. It is an area that these are patients that are being treated by multiple specialties. They're dispersed in the communities. They don't necessarily see their treating physician frequently. And some are still reticent to treat it all. And so I think that we're seeing, we've seen that certainly, but I think we're also seeing our competitors see the same.

Got it. Okay. And then can you touch on any of commercial implications possibly from a full approval of Voxogo next year? You know, could full approval meaningfully influence, you know, demand, you know, access or pricing of the product?

Maybe if I can take that first from the regulatory standpoint, I think the full approval provides three changes for the way that I think the world will view the label. Two of them tend to be rather tactical. One has to do with, again, the way that materials are reviewed by the FDA, and it streamlines them and makes them easier. Second would be on a regulatory level, when there is a full approval for an indication, that does create a headwind for new accelerated approvals in the exact same case. Though, to be fair, the FDA uses their discretion, and if they feel, again, it's in the best interest of patients, that tends not to be blocking for follow-on. The third is it gives us an opportunity to have our full data set into the label. And that is really where we see the most opportunity. Yes, there will be some physicians who I think value the idea that this is full approved. It's not on an exploratory endpoint or not on an accelerated endpoint. But more importantly, it's the details of what goes in that label. So the kind of things that are being reviewed by the FDA now are the upwards of 10 years of safety data that we have. There's 1,200 patient years of clinical trial data. That's a tremendous amount of evidence. And so in addition to the safety that that affords, and again, the opportunity to tell that story, we will be telling, of course, the height story. And that's not just annualized growth velocity, but there's an opportunity to present something that often is called final adult height, which is a bit of a misnomer. It's a defined time point with five, six years of growth, for example. Similarly, we'll be able to put forward our proportionality data, we'll look at body composition. There'll be an opportunity to have them review our frame and magnum data as well. We've got a variety of data sets, including quality of life, that will be in front of them. Again, it will be up to their discretion and our back and forth on what makes them to the label. But that will allow us not just to have medical dialogue, but the opportunity also to have our sales reps also work with the physicians and share that totality of evidence.

And what I would say is that it's not necessarily, we don't expect a change in how the medicine is necessarily used because our label really already covers children with achondroplasia that have open growth plates. But what I do expect is that it creates more confidence because of all the data that you've just described, Greg. I think that it really does create more of that confidence in the product given the amount of patient years we have, the safety, the efficacy that we're seeing, et cetera. And just as a reminder, it would be the first product that would be fully approved for the treatment of achondroplasia, which is also exciting.

That's great. Well, let's shift to hypochondroplasia, right? You made note of it. We have seen the publication just out yesterday. Maybe just from a market sizing standpoint, it would be good to have you frame the opportunity in hypochondroplasia, maybe perhaps relative to achondroplasia, not only in terms of prevalence, but, you know, also rate of diagnosis and really, you know, treatment seeking interest in patients.

And these are precisely the things that we're working on now. So as you know, I'll start off with just the prevalence, we anticipate or expect that the prevalence is roughly that of achondroplasia. And what we've shared in terms of the total addressable patient population in achondroplasia, we've shared that the global number is estimated, we estimated around 24,000. However, we've said in hypochondroplasia, we see the total addressable patient population at 14,000. And the reason for that big delta is actually the diagnosis rate. Not that the prevalence is necessarily different, but the diagnosis rate is dramatically different. The estimations now in terms of diagnosis are somewhere around 30%. We intend to move the needle on diagnosis. And that's the work that we're doing now. And Greg, I can certainly have you speak to that. So, you know, there's the work that we have to do on diagnosis, but also what you alluded to there was around also the treatment patterns and the urgency to treat. One of the most important things that we are working on now and will continue to do is to raise awareness around the condition itself so that treaters and families alike understand the comorbidities that come alongside hypochondroplasia and importantly, why the importance of treatment really is there. And so that's work that we're currently doing now. Is there anything you want to elaborate on that for that, Greg?

No, a lot of, I mean, what we would call market shaping that's gone on. That includes, again, this idea of education. But also we've been, you know, side by side with physicians, a consensus guideline for definition of the disease and how to define it is out now. And similarly, we've been working with pathologists, even on nitty gritty factors like trying to reclassify so-called variants of uncertain significance. Again, we know that there's a variety of mutations in the FGFR3 protein that cause hypochondroplasia. This is slightly different than what you see in achondroplasia, where one mutation dominates. Here, it's a big, long tail of different mutations. So clearly, making sure that that bin is accurate, those mutations, they fit into, again, this diagnosis. That's an important factor. And of course, when we start looking at efficacy, We want to make sure we see activity across all of those subsets as well. And in the publication, we had that data.

And so really quickly, just while we say the pacing of this will be in large part how fast we can drive the diagnosis rates up as well as the urgency to treat, the benefit that we have here is that we're not starting from scratch. We've built a commercialization capability in and around skeletal conditions, achondroplasia. These are the same treaters, thought leaders, et cetera. And this really, I think, does kind of provide a benefit for us as we come out and launch this product.

I was just going to add, we also have a story to tell that's not just about height any longer. This is in the publication, but we actually, type 1 error controlled, were able to show that when treated with Voxogo versus placebo during that first year of double-blind placebo control, that there was a highly statistically significant difference in arm span as well. And you may say, well, yeah, it's arms. How's that different than the legs and the height? Well, it's absolutely important in the way that these children interact with their environment. Think about combing their hair, reaching up onto a shelf, driving, these sorts of things. And so from that standpoint, we think both the payers and the patients are going to see this data set. And like we were, be quite pleased to see that there's a, you know, presuming it gets approved, a safe and effective therapy for patients. on the issue of potential approval, is full approval on the table here?

And if not, do you have clarity, regulatory clarity of what would be needed to support full approval in a, excuse me, hypochondroplasia?

Yeah, it's an excellent question. Of course, we've been talking about the full approval package for achondroplasia. And, you know, clearly there are precedents where that could set up a follow-on indication if it's closely enough related for full approval to be considered. Ultimately, that will be at the discretion of the regulators, but I just want to reassure you we're working very closely with them. We have two files that are in the FDA right now, other regions as well, and so from that standpoint, looking forward to being able to close the book again on that full approval for ACON, and again, see what comes with HypoCon. So more to come, and I think as we get more clarity from our interactions with the FDA, We'll be able to share more details on earnings calls.

Before we leave this space with scalable dysplasia, maybe we could touch on BMN 333, where you've got it to an update from the phase two study portion of the pivotal trial you're currently Maybe just you could help with sort of stage setting there, the endpoints that you're most interested in interrogating in that phase two study portion and what would you hope to see that would satisfy differentiation versus Voxogo.

Yeah. And what we know about BMN-333, number one, it was engineered to have a longer half-life. So it's got about a hundred hour half-life roughly. And it's a construct that again, releases the free CNP into the bloodstream. Think of it like a depot in that sense. So it's more of a continuous administration. That's very different than of course Voxogo that's got less than an hour half-life, more of a sawtooth pattern for PK. Now, with that continuous exposure, we ask two questions. Can we see more PK coverage safely as compared to, say, UVL? And can we see more PD, at least in the bloodstream? And the short answer is yes. We published a phase one protocol. It was at Endo this year, where we saw up to 13-fold increases in AUC for free CNP as compared to what UVL was able to produce. Similarly, that was accompanied by, you know, conservatively a two to five fold increase in cyclic GMP in the plasma. Again, it's not the growth plate, but again, it shows that there's more biology at least to be tapped into, at least in the bloodstream. So one step closer. The next step, of course, is we need to move out of healthy volunteers and we need to move into patients. We're running a study in treatment naive achondroplasia patients. So you need to, again, go to the countries where those patients exist. We're in seven countries around the globe right now. That's increasing. We're in the steep part of the enrollment curve. More to come in that regard. But that study is a classic dose ranging study. It's looking at three different doses of BMN 333, call it high, medium, and low. And we will be looking at an internal control of Voxogo there as well. Our goal is to pick a dose as compared to Voxogo that will give a high confidence in a phase three to have a superior growth profile. So what are we going to look at in that phase two to determine that? Well, two things. One is we will be measuring annualized growth velocity. We will cut the data when every patient has at least six months of follow-up. So again, it'll be more than six months in some patients. There'll be a Bayesian approach applied. There's an internal control of 10 patients on Voxogo. That will be a quick spot check. We have hundreds and hundreds of patients of Voxelgo data that we can put into a model if we need to as well. But the goal there is, again, not only looking at the dose response, but also we'll have the ability to look at exposure response, which across three dose levels of 333 is going to give us hopefully a good spread of exposure there. And with that, we would pick a dose to move forward to phase three. We'll, of course, look at safety data as well. But the phase three, as it's currently designed is a superiority study. There's no placebo. So patients either receive Voxogo or 333. And we've powered it to have 90% power to detect a 50% improvement in attributable AGV. That's not the minimum detectable number. I mean, you can back calculate the math, but it's 60 versus 60 in each arm. And again, the go signal would come out of the phase two. That phase two data will be available to us, and we would be planning to publish that. That is going to be something that we will announce sometime in 2027. Okay, great.

All right. Let's shift gears a little bit to the pipeline. I want to pick up on the Alesta ALD1 acquisition. Acquisition closed recently, right? Last week. Last week, right. Right. Just by MOA, just to be clear here, this is an ENPP1 inhibitor, if I have that correct? It is.

It's a small molecule ENPP1 inhibitor. So in these individuals, they have high pyrophosphate. That's their problem. That's a direct inhibitor of bone mineralization. And, you know, fantastic work that's been done for the field with Strindzec and the follow-on agents that are basically replacing the deficient enzyme, which is tissue nonspecific alkaline phosphatase. And at the bone, It's taking that high pyrophosphate and converting it through to its end products. You know, a lot of great work's been done there. This is a slightly different approach. I guess similar to Gaucher's, this is upstream. It's trying to deplete the substrate, trying to deplete this pyrophosphate by inhibiting the enzyme that creates an organic pyrophosphate. And that's ENPP1. A lot of good preclinical data. There's some sort of gene load cross, mouse crosses that suggest that about a 50% reduction in ENPP-1 enzyme activity can restore bone mineralization in HPP models, in rodent models. What we've seen with this small molecule inhibitor of ENPP-1 is we've seen healthy volunteer data and a limited amount of patient data. Again, looking at the PK profile, the PD profile, and the safety. And again, seeing that the molecule is meeting the requirements that we would want to see to take it forward into patients. So now, again, we are acquiring this molecule. It's finishing up its phase one portion. This is a study that's running outside the U.S. So, of course, we've got to finish chronic docs and, you know, get it filed in the U.S. But the promise here is that you don't just have a more convenient stranzeek. the promise of the molecule is that it actually will also be able to reach those compartments that aren't bone-related. So particularly the HPP patients fall into a couple different bins, a couple different buckets on when the phenotype presents itself. And particularly those where it presents later in life for the adults with HPP, many of their complaints are not the classic bone-related pathology. Instead, it's things like fatigue, malaise, muscle pain. a small molecule without the bone targeting biologic aspect has the promise to be able to target those compartments as well. So that's where we see the opportunity here. It's an established commercial space. There are established regulatory endpoints, some great work that's been done by the alkaline phosphatase molecules really to work on these patient populations, understand the endpoints. We're hoping just like they are to learn from that and again, bring patients something of value anything that you want to add christy um just in relation to the ongoing study um yeah just any uh sort of loose guidance you might offer in terms of when we would expect an initial readout and sort of the scope of that readout understanding that it's yeah uh both let me have this right is it both in healthy volunteers and in patients there are hpp patients in it and you know since the data is a week old we're still working through again And exactly how the phase one to phase two transition is going to play out, we, of course, need to engage with regulators. The short answer, though, is we plan to publish this data next year. There will be a public disclosure of both the healthy volunteer and some amount of patient data. And what you can expect is not only PK profile, but also PD, enzyme inhibition. Again, as I mentioned, the preclinical models suggest something between 30% and 50% reduction in ENPP1 activity could have dramatic influences on pyrophosphate. And again, it's been shown quite nicely by the alkaline phosphatase molecules that all of the benefits that they achieve in these older patients, we're not talking about infants, but these children through the adults really tracked with decreases in pyrophosphate. So we think of this as a fairly de-risked approach. And again, we'll be presenting that data more broadly next year.

And just in thinking about the spectrum of disease that you hope to address, particularly the sort of the older adult onset that you spoke to earlier, I guess we have a lot of development and regulatory precedent in the juvenile side, I'd imagine a little bit less on the older. Maybe you can just sort of speak to the development outlook or what development plans could look like in that segment and what you would ultimately hope to demonstrate clinically?

I think what the field has learned and it's been some great work is that these are distinct populations. You can talk about when the onset of is, is it a juvenile onset adult, an adult onset adult, you know, a teen, a pre post bone, you know, growth plate closure, all of this is important, but you have to target not only the dosing, but also the endpoint measurements to the right population. So clustering them together is probably not the right answer. So moving forward, again, we envision teasing these populations out. And then, again, the beauty of the timing of this is that we can look at those individual populations and continue to do endpoint development, particularly with the adults. Once the growth plates are closed, you can't look at the ricketts scores and so forth. You don't have that window into bone formation. So the more blunt endpoints like six-minute walk test, some of these functional endpoints have been notoriously fickle in order to see the effect of your drug. There are newer technologies that are measuring motion. There are subsets, sit to rise. There are a variety of different measures that we would intend to explore in our phase two program so that by the time we reached phase three, again, we would have solved not only the patient population question, but what's the right endpoint and what's that effect size? How do we power that study?

Excellent. Maybe, again, And moving further down the pipeline, or elsewhere in the pipeline, I should say, I want to pick up on the diomerics compound, DMN-820, and FSGS. I guess that study is now fully enrolled, and you talked about sort of a readout in 2028. That being said, right, and I guess it's on two-year EGFR that you're looking at.

I don't want two-year proteinuria.

Excuse me, excuse me. Thanks for the correction.

There's a, it's a big movement in the field and, and, you know, again, some great, Spur Sentin's done some great work, um, you know, opening this up, but the FDA now accepts two year protein URI as a full approval endpoint.

And you're right. Cause the, the question that is lingering in my mind is whether there's an opportunity for, uh, accelerated approval based on, you know, one year endpoints that are being leveraged in, you know, like diseases or diseases in this, uh, in the kidney disease category. Sorry. You know, thoughts around sort of the flexibility that you, any optionality, I guess, in the conduct of this trial where you might look to either look at data early and follow it on accelerated timeline.

So, so our current belief is that the two year reduction in protein area is the end point and it's fairly solid. Now, that being said, we have some knowledge of again, how the study is performing already. That's the study remains blinded. There was a fairly small phase two data set, because this phase three study was built upon. That being said, we know that the study has, number one, passed through futility analysis. And number two, we know that it also, you know, from the standpoint of sample size, that it's adequately powered to measure a meaningful decrease in proteinuria. So there was a formal sample size reassessment done, again, on blinded data. And the study is appropriately sized. It enrolled, it over-enrolled a little bit, I think, which is great. That was by demand. You know, patients were interested in being on the study. And again, the promise here is that an oral therapy, it targets CCR2. So the idea here is it's not necessarily a vascular targeting agent. It's targeting this macrophage induced inflammatory response that, again, leads to the destruction of some of the kidney podocytes. And the hope here is that by having a molecule that would have a meaningful reduction in protein and not have the baggage of things like a black box warning, not having the baggage, again, of having to restrict to certain levels of proteinuria, to non-nephrotic syndrome patients, that that would be of great interest to the community. Being a different mechanism of action than the pure vascular side as well, the idea of combining these agents becomes important. this study is designed to add on to ARB therapy as a baseline. So it's not displacing like Sparsenton did, you know, a prior ARB inhibitor. It's an ARB inhibitor plus minus the DMX, the VMN820 compound. And from that standpoint, again, you have to make sure you look at it through that lens. But that meaningful decrease in proteinuria is something we know the study is well-sized for. And again, a lot of promise with regard to this mechanism of action that it'll offer patients something important.

Excellent. Excellent. I'm going to end on a thematic question here. And, you know, our colleagues in tech are also running a conference this week. And so perhaps I'm asking this question on their behalf. But obviously, you know, we're often thinking about how AI, AI-enabled tools impact, you know, our businesses, all of our businesses. How is Biomarin making use of AI tools today? And how are you measuring their impact? Correct.

Yeah. And the tools can be quite powerful if you put them in the hands of the right people, you feed them the right data in the right format, and then you do something with it. And so I would say there's two places in R&D that we've really leaned into. One is reading and writing, right? I mean, we have a very document heavy work. So the idea of cutting out the white space between times, for example, when we lock a database and we file a program, it is about using AI tools to create some of those documents, the filings, but also inserting that into the workflows in the right way so people can get these work products out as fast as possible. We had a great example of a success recently with hypochondroplasia, 79 days between database lock and the submission to the FDA. That does put us in, we think, at least the McKinsey numbers, we put that in kind of the top quartile. But the whole deal is moving fast. That's great for patients. Otherwise, this is busy time, so to speak. So you can imagine having that kind of approach all along a drug's life cycle, and whether it's filing of an IND or again, filing for a new clinical trial, all of these factors can add up and reduce cycle time. I would say that the second major area that we're using AI has to do with patient finding. And in that regard, using some of these algorithms to look at very complex data sets, they might include genetic data. So looking for hotspots around the globe, they may include social listening and, again, the activities that are going on where we know that patients who are quite educated are seeking out information. They're just not finding their way to a physician. And then, of course, the opportunity to do good old-fashioned looking at claims databases and so forth. That does allow us to find patients not only in the commercial sector, but also for our clinical trials. And we have some great examples where we even found a patient who was an in utero patient. It was a mom looking up for hypochondroplasia on the internet. And again, she was forwarded to one of our clinical trials. So they work. It's very helpful. I would say that the area that I would love to see us lean into more, and we're dipping our toe here, is giving these tools to the scientists and allowing them, again, when it comes to molecular design, organic chemistry and amino acids are another form of a language, right? So the large language models do a good job creating some of these reagents. That'll hopefully cut down the time and the number of molecules that we have to test as we go through our own funnels to bring these things into the clinic. So we have the luxury at Biomarin of, you know, we have some resources. Again, with all the work we've been doing, we have about a billion dollars of free cash flow a year. That means that we don't always have to be on the bleeding edge of these technologies. And we're finding that there's a very vibrant third-party sector. They've battled it out for the winners, but for writing things like clinical study reports, we're able to actually test a couple of them and see which of these tools is the one that works best for us. And we're finding that, you know, in addition to some of our work with Viva and so forth, getting our data lined up. I do think that there's a major opportunity here to do more with less. And, you know, as an R&D guy, I've got a budget and I need to get as much activity into it and get as much to patients as I can. And that's really the name of the game right now. Technology is part of it, but it is enabling the people who have the creativity to do the work.

Great. Well, that's a good note to leave it on. Thanks so much, Greg and Kristen, for your time today. We really appreciate it.