Welcome to the Morgan Stanley Global Healthcare Conference. I'm Jeff Hung, one of the biotech analysts. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. For this session, we have PTC Therapeutics with CEO, Matt Klein. Welcome.
Thanks, Jeff. Great to be here.
So for those who may not be as familiar with PTC, can you just provide a brief introduction?
Sure. PTC is a global biopharmaceutical company that discovers, develops, and commercializes innovative therapies for patients with rare disorders. We've had a very successful 2024 thus far. We recently updated our 2024 revenue guidance to $700 million-$750 million, and closed the second quarter with over $1 billion in the bank. It's also been a year of excellent execution across the company. We've already submitted three drug approval applications to the FDA. The first was for our gene therapy for AADC deficiency. We recently held a late-cycle meeting with the FDA on the BLA, and it was a successful meeting, and we're on target for a decision from FDA in November. We submitted an NDA for our PKU program that I'm sure we'll have the opportunity to talk a bit about.
This is highly differentiated therapy that easily represents over a billion-dollar commercial opportunity for us, and we are expecting a decision on filing from the FDA by the end of this month. We resubmitted the NDA for Translarna to the FDA. We recently heard back from the FDA. They've asked for some additional information for us to provide them before they begin their review, and we'll provide an update on the timeline once we have it, and we're on schedule to submit the NDA for vatiquinone for the treatment of Friedreich ataxia before the end of the year.
In the second quarter, we read out results, interim results from our PTC518 program for Huntington's disease, where we demonstrated continued safety, continued dose-dependent lowering of mutant huntingtin protein in the blood and the CSF, that being the causative agent for the disease, and also showed early dose-dependent effects on important clinical measures. This combination of safety, biomarker effect, and early clinical signal has really put PTC518 as the leading therapy in development for Huntington's disease. We're also on schedule to share results from our potential registrational study of utreloxastat for ALS in the fourth quarter. A very busy year. We continue to execute on all fronts, continuing to have commercial success and really building a strong foundation for future growth and success.
Great. Let's start with sepiapterin. Can you just walk us through the unmet need in PKU and the treatment paradigm?
Yeah, absolutely. So this is our program, sepiapterin, for the treatment of PKU. And PKU is a little bit misunderstood because while there's two approved therapies, there's still a significant unmet medical need. It's estimated in addressable markets as about 58,000 patients, approximately 20,000 patients in the U.S., and only about 10% of those patients are on current therapy. So that leaves a very large population of patients, both pediatric and adult, who are in need of a highly effective, safe, and tolerable therapy. Sepiapterin is an oral therapy. We shared results last year from our phase 3 AFFINITY study, in which we demonstrated highly statistically significant and clinically meaningful effect, with a mean reduction in phenylalanine of over 60% in the overall population, and 69% mean reduction in classical PKU patients.
That's the more severe patients who are not met by current BH4 therapies. We also reported that we had over 84% of patients meet guideline levels for phenylalanine, which is less than 360 micromole per liter, and we had 22% of patients who had normalization of phenylalanine levels, which is almost unheard of in these clinical trials. We also were able to get a look at patients who are on Kuvan currently. We had 29% of those patients enter the study. They got washed out of Kuvan, then put on sepiapterin, and we had almost 50% further reduction in phenylalanine levels. So all of these data support that this can become the standard of care for PKU.
In addition, following the placebo-controlled AFFINITY study, patients rolled over into a long-term open label extension, which allowed us to demonstrate durability of treatment effect and safety, which we're doing, and it also allowed us to answer a very important question, which is: Can sepiapterin allow patients with PKU to liberalize their diet? Can they take this drug and get off their highly restrictive, debilitating diets and enjoy higher protein in their everyday life? The short answer is yes. We have patients in that open label extension in the Phe-tolerance protocol, and what we've found is about 60% of patients are able to take protein beyond the levels recommended for you and I. This is transformational for patients.
It allows them now to have regular diets with regular protein intake and still have phenylalanine control, which is really the holy grail for PKU patients, and obviously is incredibly important for physician uptake and payer discussions. So we really have a very strong data package showing a high degree of efficacy, safety, and tolerability, and as I mentioned, that NDA was submitted. We've also submitted the marketing authorization in Europe, and it's under review there. We've submitted the authorization application in Brazil. We're expecting to submit in Japan later this year. So all things are in position for a global launch. And given the size of this population, the still significant unmet medical need, and what we think we can achieve with pricing, that's why this is easily a billion-dollar-plus opportunity for sepiapterin.
Could even be that high in the U.S. alone.
... How are you thinking about the label as it relates to dietary phenylalanine restriction? You know, is the ability to liberalize diet something that you expect could be included in the label?
We've included the Phe tolerance data in the applications. We'll obviously get a better idea of the label as we get closer, but we still have those data, and they'll be very important for physician uptake and for payer discussions. I think what people don't understand how debilitating PKU is and what it means to have a phenylalanine-restricted or protein-restricted diet. What patients require is being on specialty foods that have very little protein. It might be that their protein allotment for the day could be one egg. That's it, for the whole day, or one piece of toast. That's it for the whole day.
The reason why the majority of patients are not on therapies is because, for example, Kuvan has not been able to demonstrate that patients can take the therapy and liberalize their diet and have more protein in their diet. So obviously, if you're a patient and you can't get off that highly restricted diet, there's not a big motivation to take a therapy. And that's why our ability to show that sepiapterin is allowing patients to do this and allowing the majority of the patients to take protein in excess of what would be recommended for a non-affected individual is so important for patients and will be ultimately so important for the uptake of patients and the success of the therapy.
You kind of touched upon this, in your previous response, but what is your latest thinking on pricing dynamics and market uptake against the approved drugs?
Yeah, I think the first and most important point is that the vast majority of patients are not served by the current therapies. The other important dynamic here for PKU is that well, the essential pillars for commercial success are already established, right? So there's newborn screening. So patients in the U.S. are diagnosed, U.S. and many countries around the world, diagnosed at birth. They know they have PKU, right? Very important. Two, since there are available therapies, there are centers of excellence established. There's centers of excellence that have physicians and nutritionists who are experts in managing PKU. They know where the patients are. These patients are tied to expert centers, and importantly, we know where they are.
So our teams have already worked to identify the, these centers of excellence, who are the prescribers, who are physicians who used to prescribe therapies but no longer do. You know, we're able to map all this out very easily. The next is payers understand it. They know exactly what they're going to look for, and an effective PKU therapy is going to lower phenylalanine, and it's all set up, and it makes those discussions very easy. So you have all of the kind of hard work we usually have to do when we think about a rare disease launch in place. All that's needed is a highly effective and tolerated therapy, which we believe sepiapterin can be and become the standard of care.
And could you just talk a little bit more about your commercial launch preparation activities and, you know, what's already underway versus what you might hold off until approval?
Yeah, so we're well on our way. As I mentioned, we're in this unique situation where we don't have to do all the work of patient finding and who are the KOLs and where are patients being treated. That's all been mapped, and in fact, when we started the phase III AFFINITY trial, one of the things we were certain to do is to include these centers of excellence in the trial, so get the KOLs who have patients with PKU already attached to the therapy and get involved with studies, see firsthand how effective this therapy can be and how transformative it can be for patients. In fact, when we opened up the open-label extension trial, we also allowed patients to be directly enrolled in an effort to get more global centers of excellence involved in the program, so that started early on.
As I mentioned, our teams have worked hard to map where the centers of excellence are, map where the physicians are, understand where patients currently on therapies are, where are patients who've been on therapies but no longer on therapies, where are they at? So we have all of that mapped. And then we have an outstanding patient engagement team who's also been working very closely with the community to understand what are the needs of the patients, how can we support patients in their entire PKU journey, not just in regards to sepiapterin, but what we always do in rare disease, which is perform a very important role in being supportive to patients. So all of these critical activities are underway. They're continuing.
We've had initial discussions with payers as well to understand what those discussions could look like, in an environment where there are existing therapies. So, I think our commercial teams would say they're ready to go. They just need the approvals to launch.
You talked about the different mapping that your teams have done, including the patients. Is there a patient segment that you're initially focused on, or expect to see the most demand at launch?
Yeah. So when we think about the segments, there are a few important segments in PKU. There's the patients who are therapy naive, which is about 30% of patients, and these are usually patients who have classical PKU, who the physician never thought would benefit from therapies. Then there's patients who've tried the existing therapies and failed. And then the third segment is that small segment of patients who are still on therapy. When we started, we thought that the initial low-hanging fruit, if you would, would be those patients who are therapy naive, who never believed they'd benefit from a therapy. And then when you see that we have classical PKU patients, those more severe patients, having a 69% reduction in phenylalanine, that we thought that would be the first priority access segment to access.
It is a priority segment to access, and it is one we're going to go after. But what we've also heard from physicians, in fact, we had a deep dive last year where Ania Muntau, who's one of the leading KOLs for PKU, she said, "I'm going to try all my patients on it." Because if patients have had benefit from existing therapies, we have 100% confidence based on the mechanism of action of sepiapterin and the data we've collected, that they'll do even better on sepiapterin. So we're seeing now that other segment of patients who are on therapy, the potential for switches, also could be one that we could access early. I think the good news here, Jeff, is that we have a data package that suggests that we can address all of those segments.
So it's a matter of just getting to all those patients and working to get them on drug as quickly as possible, and which is what our teams are set up to do and are working on right now.
You've emphasized the blockbuster potential with sepiapterin. You know, how are you thinking about Europe, Asia, and Latin America? You know, is there an area where you're expecting to see greater growth, potential, or patient demand?
Yeah. So one of the things we've thought about with sepiapterin is it's gonna be a true global launch. I mean, this is a worldwide problem, and PTC has a global commercial infrastructure. We have a footprint in over 50 countries. We've been able to deliver therapies to patients with rare diseases in all these countries. So we have an infrastructure built already in all of these different countries to make sure that we can optimize getting patients on therapy. I think one of the exciting things about this opportunity is that the revenue opportunity is so large, and we have the infrastructure. There's minimal incremental cost, if any, for us to successfully launch this.
And so we'll look to have the success in the U.S. that we talked about, but also in Europe, in Japan, in Latin America, in Asia, Middle East, North Africa. All the regions where we are now, we're gonna continue to work because we have the infrastructure. We again have done the similar mapping and understanding where the patients are. So the reason we see the blockbuster potential is not only on the huge market opportunity in the U.S., but because we can access the global opportunity.
Great. Maybe moving to PTC518, for Huntington's disease. You talked a little about, you know, some of the data that you've shown, and I don't know if there's any other aspects of the data you'd like to highlight, but you're planning to, you know, meet with the FDA to discuss the potential for huntingtin lowering to serve as a surrogate endpoint, in the context of accelerated approval. So what is this based on, and how confident do you feel in being able to demonstrate the connection to therapeutic benefit?
Huntington's disease, of course, is a horrible neurodegenerative disease. It's autosomal dominant, which means if mom or dad has it, the kid has about 50% chance of having it, so it's got a significant prevalence. But it's also unique in when we think about neurodegenerative diseases, in that it's monogenic. Every patient who has Huntington's disease, whether a juvenile or adult, has it resulting from a mutation in the huntingtin gene. And it's also unique because we know what the heck causes it. We're not in a situation where we don't know what causes the majority of Alzheimer's disease for patients or even Parkinson's disease for patients. We know that this is caused by the production of a mutant huntingtin protein that is toxic to cells, leads to cell injury, cell death, tissue loss, and progressive neurodegeneration over decades.
And so what we do with PTC518 is it's an oral molecule that leverages PTC splicing technology that brought us Evrysdi for SMA to decrease the production of that disease-causing protein. So again, we're in this situation where we know what causes the disease, and we're targeting it. And so that, that's very important to the overall treatment hypothesis. What we've been able to show in our studies is that we're able to effectively lower huntingtin protein 20%-50%, which is the range that's been demonstrated in the literature to be associated with clinical benefit. There's a large literature showing exactly what one would expect, that if you decrease the amount of this protein, you have benefit.
And that's been shown in animal models, as well as in an epidemiologic study where patients who have a single nucleotide polymorphism, such that they make 50% less protein, have about a nine-and-a-half year delay in onset of disease and a slower disease progression. Direct evidence that reducing huntingtin protein has significant benefit on disease course. Now, to the question of accelerated approval, this all becomes very important because when you read the guidance for a surrogate endpoint for accelerated approval, you have to be able to demonstrate that change in your biomarker is likely to have clinical benefit, one, and two, that the magnitude of effect you're recording in the clinical trial is that magnitude of effect that is likely to have clinical benefit. So when we apply that to huntingtin lowering, both boxes get checked.
There's a wealth of scientific literature, in addition to just scientific logic, that if you have a disease-causing protein, less of it's gonna be good. There is evidence showing that lowering it has benefit, and lowering it in that range of 20%-50% is the magnitude of effect that has been associated with that benefit. And so what we've been able to do in PIVOT-HD is show that we can have the dose-dependent lowering, achieve lowering within that magnitude, be able to show that we're having early biomarker effect and clinical effect that would be significant. So we believe that combination of existing scientific literature, just the scientific realities of HD causation and pathogenesis and what we've seen thus far, really can make this a compelling package.
We're in the process of submitting that meeting request to FDA, and we've shared that we plan to have that meeting in the second half of this year. It could be very important in achieving alignment on a potential surrogate endpoint that could support an accelerated approval application.
Now, you're also working on the phase three trial, which could serve as a confirmatory study or registrational trial. Are there any updates that you can share there?
Yeah. So we shared after we read out the interim report from the PIVOT-HD study, that with those twelve-month data in hand and the evidence we now had, that the drug was safe, well-tolerated, had the mechanism of action it needed to have, that is, lowering huntingtin protein, and we're seeing early clinical effect, that we had all of the boxes checked that we needed to move confidently forward with the design of a phase III efficacy trial. So we are also in the process of getting ready for a separate Type C meeting with FDA to discuss an endpoint strategy for the efficacy trial. Again, whether that would be a confirmatory study in the context of accelerated approval or whether that would be the registration trial itself.
So we look forward to having that interaction with the FDA also in the second half of this year, so that we basically are in a position to understand what we need to do next to move this program forward.
Okay, great. Maybe moving to Translarna, where are you in the process with requesting the re-examination of the CHMP opinion, and what is the process from here?
Yeah. We submitted our grounds for re-examination this week, actually. The re-examination process is typically about 120 days starting from the day that you get the negative opinion onward. Day 60, which was this week, we have to submit the grounds for re-examination, which is basically a briefing package, in which you address the concerns that were raised by the CHMP in their review and negative opinion. So we've done that. There'll then be a review by CHMP. As part of the re-examination process, new rapporteurs are assigned, so that it's basically a new review of your data. And that process is expected to take about 60 days.
We are now in a process where we're just waiting to hear back from the CHMP and understand what that timeline could look like.
Can you just remind us what percentage of sales for Translarna is tied to the EU?
Yeah, so as we talked about in 2023, it was less than 50% of sales were tied to EU. Translarna, when we started, obviously, Europe was the first place we commercialized Translarna, and that made up the vast majority of our Translarna revenue. But over time, we've expanded the geographic footprint to regions around the world, and that proportion of revenue from Europe has gone commensurately lower, become lower and lower.
On that topic, I guess, can you just remind us how your international expansion is progressing, and are there any updates that we should be expecting there?
Yeah, so right now, we're focused on obviously being able to garner as much revenue we can out of Europe. The re-examination, the European Commission not adopting the CHMP's opinion and sending it back has allowed us to continue to get revenue in Europe, and we believe with the timeline for the CHMP re-examination and the subsequent 67 days needed for EC adoption of that opinion, even if the opinion stays negative, we should have revenue in Europe throughout the year, and we're seeing patients continue to stay on the drug. There was even a period where we saw new patients added, so that revenue is in place, and as well, outside of Europe, we're continuing to see patients on drug.
In terms of geographic expansion, we obviously have had the U.S., which would probably be the most significant expansion we could do, for Translarna, and then there's other regions, in Asia-Pacific and elsewhere that we're continuing to look at opening up, access to the therapy there.
You mentioned that you've resubmitted the NDA for Translarna in the U.S. Can you just provide more color on the market opportunity here compared to Europe?
Yes. So we've always believed, for a number of reasons, that it could be a market opportunity that could be a multiple of the European opportunity. We're in a situation where we have about 150 patients on Translarna now in the U.S., who've been on it for many years. So if we had the ability, in the context of an FDA approval, to finally launch Translarna in the U.S., this would be a pretty rapid ramp for us. We obviously have teams, customer-facing teams with expertise in DMD. We've been commercializing Emflaza in the U.S. for a number of years. We know the physicians very well. We know the patient communities very well. PTC was the first-ever company doing drug development in DMD, and those relationships are long and strong.
We also know that a vast majority of nonsense mutation DMD patients may not be addressed by gene therapy, so we see this as a very real market opportunity. We resubmitted the NDA. I mentioned that the FDA has asked for some additional information that they said before they begin their review, and we'll have a better idea on timelines in the coming weeks.
Then given past feedback from the FDA, as well as what you've just talked about in terms of, you know, the additional questions or information that they've sought after, you know, what gives you confidence in potential approval in the US?
Yeah, we've spent a lot of time, and we're very wary of the history of Translarna in the US, and we wanted to make sure that we worked collaboratively with FDA to understand what would a package look like that could stand for approval. Study- 41, which was the most recent placebo-controlled trial, is a strong study. In the ITT population of 359 boys, we have been able to demonstrate statistically significant effect on six-minute walk test, North Star, time function test, time to loss of 10% ambulation. I mean, that consistency of significant effect is something that's not really been seen in any DMD therapy, even ones that have been approved by FDA.
Then we also have the STRIDE registry, which is our long-term real-world evidence, where we have over five years of follow-up and over 300 patients and have been able to demonstrate that we have a delay in loss of ambulation of three and a half years. So we're able to show that the effect that we're achieving in the time-limited clinical trial is manifesting cumulatively and a significant delay on the critical morbid milestones of the disease. And so that's the package we discussed with FDA that they had shared with us, they believe would be reviewable. And given the significant unmet need for nonsense mutation DMD patients, we believe that there's an opportunity for approval here.
You know, we have always said that we will do our best and make every effort to try to bring this therapy to boys with nonsense mutation in the U.S.
Now, vatiquinone for Friedreich ataxia, you know, with an NDA submission by year-end, can you just talk more about what the submission will consist of, and are there any remaining data to be collected?
Yes. So again, we've worked collaboratively with the agency to understand what could an NDA package look like for vatiquinone for the treatment of Friedreich ataxia. The foundation of that NDA will be the placebo control results from the 72-week MOVE-FA trial, where we had a statistically significant effect on the upright stability subscale of the disease rating scale, known as the mFARS. The upright stability scale is the most sensitive, in fact, the only sensitive, component of that scale for pediatric and young adult ambulatory patients who were the primary analysis population of the MOVE-FA study.
And to be able to show significant effect on upright stability, which has been associated with a risk of loss of ambulation, allows us to say that we not only have a statistically significant, but a clinically significant effect on something critically important for ambulatory patients with FA, and that is loss of ambulation. Along with the effect on upright stability, we also had benefit on walk distance as well as fatigue, putting together a collection of evidence from MOVE-FA that is persuasive that we're having a meaningful effect on the disease, so that'll be the basis of the NDA. In addition to that, we're providing confirmatory evidence from three sources. The first is the long-term open label extension of MOVE-FA.
This is where we're gonna look at treatment of patients, of those initially assigned to drug over three years, and comparing the treatment effect in those patients to a propensity-matched natural history cohort. This is very similar to the confirmatory evidence that Reata used for the Skyclarys approval. We also have a second source of long-term data from an earlier placebo-controlled study in adult patients, where we have twenty-four months of treatment data, and those patients will be compared also to a natural history match cohort. There was a previous publication that showed a highly statistically significant benefit of drug relative to natural history, but in our discussions with FDA, they asked us to provide a new analysis plan and redo that analysis. So that is in progress now as well.
And in the third bucket of confirmatory evidence will be mechanistic data that we have from a number of preclinical studies, which demonstrates that vatiquinone has a meaningful effect on biomarkers of the disease that are referable both to the mechanism of action of vatiquinone and also to Friedreich's ataxia pathology.
How is vatiquinone differentiated from existing therapies, and just how are you viewing the market opportunity?
Yeah, absolutely. So, vatiquinone has the benefit of having a very strong safety database that's been generated in patients of all ages. In fact, we've treated patients with vatiquinone as young as one month of age. So being able to have a therapy that could be used by the entire Friedreich ataxia population would be incredibly important. The only approved therapy now, Skyclaris, is approved only for 16 and older. So to have a therapy that, again, could be for younger patients and adults would be very useful, and also to have a therapy that has a data package centered on the ability to preserve ambulation would be unique and also incredibly meaningful for Friedreich ataxia patients, because loss of ambulation really is the first key morbid transition point in the disease.
Now, for utreloxastat, you know, you have phase II data, you know, reading out later this year. Could you just talk a little bit more about the powering assumptions for the study and what you're hoping to see with the data? You know, like, what would be a positive result?
Yeah. So utreloxastat targets ferroptosis. It's a 15-lipoxygenase inhibitor, and ferroptosis has become increasingly demonstrated to be a highly important pathway underlying neurodegenerative disease pathology in general, but specifically ALS. There's a large volume of evidence showing that you can target ferroptosis and affect a lot of the different important aspects of ALS. So this is a phase II study that was designed based on guidance from the FDA to be able to stand for registration if positive. So success here would be a statistically significant primary endpoint, which could allow us to submit an NDA for ALS in 2025. We've powered the study to have 85% power to demonstrate a two-point difference on the ALSFRS scale, which would be a magnitude of effect considered to be meaningful and could stand for approval.
Great. Ahead of the Upstaza PDUFA, can you just talk about your commercial launch preparations?
Yeah, absolutely. So Upstaza is a gene therapy being developed for AADC deficiency, a very rare disease where kids are born without the enzyme that allows them to make dopamine. In the absence of dopamine, which is the neurotransmitter responsible for motor function, these kids have no motor function. So in the most severe cases, they never gain the ability to lift their head, to swallow, to sit up, to crawl, nothing, and typically die in early childhood. And this is a highly innovative gene therapy product because we are able to provide the enzyme that will allow kids to make dopamine, and we deliver it through a neurosurgical procedure to the exact location in the brain, the putamen, where it has to do its activity.
So this is an innovative product that combines a, I say, minimally invasive neurosurgery, and people kinda say: How can a neurosurgery, brain surgery, be minimally invasive? But it is as much as it can be, because what we do is we rely on MRIs to provide a Google map that guides the surgeons to go from outside the child's head to the exact location where the gene therapy is administered. And what the data have shown is that in delivering the gene therapy, within a short period of time, weeks, the children start to make dopamine. We can see that on radiographic scans and also on measuring dopamine levels in the spinal fluid, and then sequentially develop motor function. First, the ability to lift their head, then to sit up, then to crawl, and eventually walk. And it's truly transformational.
So the t here's a mismatch between how transformational this therapy is and the real small population size, but we look forward to trying to get this therapy to every patient in the U.S. who can. We've worked hard to leverage the lessons we've made from the European launch in preparing for the U.S. launch, we've identified our centers of excellence. These are neurosurgical centers of excellence, where the surgeons are able to perform that special stereotactic procedure that's needed to safely deliver the therapy.
What we did is in our clinical study that we did, our Study 042, which is part of the NDA, BLA rather, we included these centers in those studies, so that way we were able to get the centers, not only the surgeons, but the nurses, the pharmacists, the physical therapy staff, the ICU, to have everyone involved in this procedure familiar. So again, we're in a situation where the centers are ready, patients are ready, and our teams are ready, pending that, what we hope is a BLA approval in November.
Maybe one last question in the last few minutes. You talked about how you've tried to apply learnings from the launch in Europe. Are you expecting any differences in the launch or patient dynamics in the U.S., you know, compared to Europe?
Yeah, I think one of the—we talked about what we did in Europe. There are three components to our launch plan in Europe. Again, a lot of it's centered on this concept of centers of excellence, where it didn't make sense, given the small population, to put centers of excellence in every single country. So we said we were gonna rely on three pillars. One would be, you know, centers of excellence in country with pricing and reimbursement and treatments there. Second was going to be cross-border health, where we would basically say, "Okay, we're not putting a center of excellence in every country, but there may be kids in one country that we can then bring to a country where there is a center of excellence." And we've leveraged that pathway very well in the European launch.
And then the third is, leveraging early access pathways that would allow us to treat patients before formal pricing and reimbursement were set. The U.S. is gonna be a slightly different paradigm because it's one country. We'll have centers of excellence spread out geographically, so there'll be a need to get a patient maybe from their home state to a center, but it's different. There's no cross-border considerations. We're not gonna have the early access pathways. This will be straight up, traditional access and patient treatment.
Great. We'll leave it there.
Okay.
Thank you so much for your time.
Great. Thank you very much, Jeff.