Beam Therapeutics Inc. (BEAM) September 9, 2026 Conference Transcript

I'm Sam Semico, one of the senior biotech analysts here at Citi, and it is my pleasure to be hosting BEAM at Citi's 2026 Biopharma Back to School Summit. I'm joined by John Evans, CEO, and Shravan Amani, CFO. John and Shravan, welcome, and thank you both for being here.

Thank you for having us.

So why don't we just start by level setting? You know, you've made a lot of progress across the pipeline this year. Just tell us where the company stands today and what we can expect through the end of the year and beyond.

Yeah, great. So Beam has made a lot of progress. We're moving very quickly now across a broad range of programs, all building off of this very dynamic platform that we've created using base editing, of course, next generation CRISPR 2.0 technology for more precise gene editing. but then building that into a delivery and manufacturing machinery that that is now quite mature so doing both ex vivo cell therapy but also now in vivo lipid nanoparticle part programs and manufacturing all of that internally so it's a very insignificant capability we've built the programs are now moving very quickly so risk to sell our sickle program is really awaiting its final data cut from a now fully enrolled and dosed beacon trial. That will become a BLA filing right around the end of the year, which will be our first BLA. So that'll be an update we're excited to share. Then in the in vivo programs on the liver, we have beam 302 for alpha 1A trypsin deficiency. We just have shared sort of new data. They are showing really, you know, really dramatic consistency of that program as we continue to add patients. That's now in a pivotal cohort. We're enrolling patients. We dosed our first patient in July. By the end of the year, we hope to significant progress on enrolling that 50-patient cohort and continue to move that program forward towards patients. Behind that is BIM301, which is a program for glycogen storage disease 1A, the RD3C mutation. There we'll have first data, first in human data this year on a couple of dose cohorts for that program, another sort of metabolic type of mutation that we're going to try to correct. And then finally, also in vivo PKU, BIM 304, we now have an open IND. So we're now opening sites as we speak and hope to begin screening patients towards the end of this year. And obviously then that'll become a clinical program to follow. So lots going on, lots to talk about, but we're seeing this flywheel continue to gain momentum on both the payload technology and our delivery manufacturing capabilities.

Yes, absolutely. So as you said, lots to get into. Why don't we start with AATD? So yesterday you did share new data at ESR, an updated data cut. And our takeaway, kind of what you said, is that it seems to be quite durable and that the level of AAT and MAT induction that you're achieving just continues to be within the range of that protective MZ phenotype. So maybe it would be helpful just to hear a little bit of the feedback from ESR. Walk us through how physicians are viewing the data, how impactful they believe achieving these levels of AOT and MIT are for patients.

Yeah, it's a great question. So there's been a lot of enthusiasm, and I'd say ERS is no exception. We're hearing from physicians around the world, certainly our investigators, but more than that, that this looks like the profile they've been waiting for. You know, this patient community is really overdue for some better therapies. And, you know, when you ask them sort of what is the ideal outcome, they will say, well, we need something that raises our AAT into the protective, you know, above the protective threshold, which basically means into the teens, because that is the place where there are no patients who have those kinds of levels. We want to raise it by creating M, the normal protein, which we know is functional and will protect their lungs. At the same time, we want to be reducing Z as much as we can. That's a toxic protein, both for the liver, but we've learned a lot more recently about its disruptive effects systemically, causing inflammation and interfering with the protection of normal AAT. You want it to be inducible, right? So when you get sick, it needs to go up, and we have shown that. And then, of course, you want it to be durable. You know, patients, these patients have been on chronic therapy their whole lives, taking weekly augmentation. They're very hungry for a one-time cure, and that is what we believe we're offering. So lots of excitement, I think, across the physician and patient community, and we continue to see that operationally in our BIM-302 trials.

And so one thing we heard after the presentation yesterday is maybe a little bit of confusion on the assay used to quantify AAT and MAT. It can make cross-trial comparisons perhaps a little difficult and maybe even comparing your own data cuts difficult. So maybe just talk about whether turbidity or LC-MS is the better assay, why you're using both, and maybe clarify if we're seeing a decrease in AAT levels or if it's just an assay difference?

Yes. Great question. So, um, so there are multiple assays available. Um, you know, and I think the, the important point is to step back and see that they're actually telling the same story across the board. Um, we do change back and forth between a bit. So, so turbidimetry is the classic in the field. This is literally taking protein in liquid, shaking it up and seeing if it disrupts light scattering. Uh, so it's a, it's a fairly crude sort of old assay, but it is used by the clinicians very frequently. So that's the standard. If you're going to get diagnosed with ATD, you're going to use turbidimetry to do so. But they don't check ATD levels very frequently. It's kind of a one-off. So for our first academic conference presentation, which was yesterday, we thought turbidimetry makes sense because it could be familiar to the clinicians and they would fully understand it. LCMS is different. That's, of course, mass spec. And we need LCMS to discriminate between the kinds of AT. right so if you want to see how much m you have how much z you have a turbine imagery can't do that so we need lcms at least for that um and so you've seen some of our lcms data reporting that our expectation is ultimately even things like total at level for the fda they will also want lcms and so we have been bridging our way over to that um to that assay um i expect we will you'll see more of that from us in the future right now we're validating it for pivotal stage um but you know it it gives fairly similar answers there's definitely for these assays there is a you know 10 wiggle as you as you think about um sample to sample and also at levels themselves drift up and down for these patients on on that order of magnitude so i definitely don't see there's no change in our levels i think that you should interpret here um you know between 16 14 and a half you know it's all basically mid-teens and i as we have seen it's quite durable so once you see those set points, I think you'll see them sustained.

Right. Okay. Yeah. What patients tend to achieve is what they tend to keep.

Exactly.

And so then looking forward, there's a lot of competition in AATD. The space has quickly become quite crowded. You remain well ahead of competitors entering pivotal studies, but other companies are also developing gene and anything therapies. And so how do you see 302 positioned, you know, outside of being first to market against all the competition?

Yeah, so I think, you know, the success of being 302 is definitely going to invite competition, and they will be coming. We have the fortune of being well ahead. So we've been up against some different classes of medicine. So RNA editing is one that we've been facing. I think we're now moving past them in operations. We're now into pivotal trials. RNA editing is still more of the early stage development. By and large, the numbers they've produced have been positive, clearly, for patients, but maybe numerically not where we're at in terms of both levels of AT, amount of M being produced, amount of reduction in Z. So then you look to the DNA editing field. And as I said, I think the DNA editing is maybe more where the ideal target product profile lives for the patients and for the community. And there, as you noted, Beam3R2 is in pivotal trials. We will have a clear first-in-class advantage. We're, you know, about two years ahead of our most advanced competitors, but there are going to be others. You know, by and large, it isn't clear to us where the opportunity for differentiation clinically really lives. There will definitely be a competition around, you know, who can maybe have the higher AAT level. And that, you know, that'll be something that people focus on. The reality is all of our patients are already above the protective threshold, right? So there's no evidence that there's any clinical difference, you know, once you get to that state or going a little bit higher. It also isn't clear to me exactly how much higher you can go. I think we'll learn as we see some of the competitor data. but i think it's clear to me that that you know editing a lot of the liver in these patients you can get patients to that protective threshold you can get them into the teens i don't think it's going to be possible to get people to 30 you know which is kind of where normal would live but but again it's all good because patients are protected now beyond that i think beam throw two is doing everything we needed to do so i think we're you know we're looking forward to pressing on the accelerator and staying certainly ahead of the competition and bringing, you know, a new product to patients as quickly as we can. All that said, competition is good for patients, you know, we're always welcoming of more entrants, they certainly deserve more options.

And just, you know, maybe double click on that a little bit about the AAT level, you know, I mean, do physicians recognize that there is it's going to be difficult to, you know, show clinical differentiation, say if you have 20 AT versus, you know, your 14, 16, depending on the assay? Like, how do you think it'll be viewed, like, by physicians when they're trying to make treatment decisions?

Yeah, I think it's actually quite well understood. So these physicians have thought a lot about the clinical genetics here, right? So ZZ is the profile of a patient. They live in the six, you know, five, five, six range in terms of their alpha one levels. And their parents, right, the people who or carriers who maybe have one copy of Z, but the other is of M, they are in the teens. And this is called MZ. And so an alpha-1 expert intimately knows what a ZZ patient is like versus an MZ carrier. And then of course, MM is the normal. And there's been extensive literature that these community groups have done to understand what is the relative risk of each of these groups. And it is a very settled question that MZs do not have progressive disease. They're perfectly stable, where they may have a little bit of higher risk is if they are heavy smokers, for instance. So if you have a second hit, you can see a little faster decline, but that's really the extent of it. So I think at the end of the day, I think if we're all in sort of the MZ neighborhood or better, I think that that's going to be a wash from a competitive perspective.

Got it. Okay. And then how important is it to lower Z levels? Does Z have its own pathologic effects?

It does. And I think that is actually an increasingly important part of the story here, where, of course, we want the total alpha-1 levels to go higher. And then we like the fact that it's inducible. So when you get sick, it goes even higher still. But it's really the quality of the AT that is being produced in the body, meaning in our case, we're getting 93% M circulating and only 7% Z. And that's because we have lowered Z by about 84%. That's really helpful. It's helpful, obviously, to the liver, because Z is the thing that's building up in the liver and causing toxicity. But it's increasingly clear, and Dr. McElvaney, who was on our call yesterday morning, was speaking to this, that Z is a bad actor systemically. It causes polymers, and those polymers are basically inflammatory, and they lodge in tissues, and they cause a lot of local inflammation, they can also, you know, bind to and actually, um, inhibit, uh, the, the, the natural AT from doing its job, uh, to, to, to stop neutral last days. And so they can actually frustrate M from doing its job. So I think there are lots of sort of emerging ideas that the less Z you have, the better systemically. And so our ability to do that is, is an important part of the product profile.

And so how is enrollment going in the pivotal cohort? I feel like you've commented that it's going quite well. I'm wondering if you just like speak to some of the engagement that you're hearing from your investigators, you know, based especially on the back end of this updated durability data.

Yeah, it is going well. I think we have great enthusiasm. We're at 14 sites across six countries now. We've been adding more sites in the U.S. in response to demand. And yes, as I noted, there's, you know, almost each site has a list of patients who are interested and are willing to travel for this therapy, I think it's very clear we've gotten on the map with the community. So, you know, nothing more to say other than we feel confident in the enrollability of the cohort and it's moving quickly.

How long does it take to get a patient off the list and, you know, into the trial? Is that site dependent on their capacity or is it your ability to, like, be able to dose them? How does that work?

Yeah, it's more the, I mean, the site obviously has capacity. They have to work through it. The patient has to go through screening. I mean, that's probably the biggest thing. So we just have to make sure they meet the inclusion criteria, that they're stable and all the right medical things are checked. You then have to wash them out, right? So they're generally on augmentation, particularly in the U.S. And we are washing those patients out. So you want to get the augmentation out. That then gives you a clear view of their true baseline in terms of alpha-1 levels, all z of course then we take a baseline phase right so then we're going to take a series of measurements to make sure we have a good average of what their their set point is uh and then you can treat so i think there's there are definitely a few steps that to go before the dosing but as i said we're already in the dosing phase we had our first dose in july so this has all been ongoing now throughout uh 26 and it's a little early to maybe start this conversation about uh the commercial strategy, but, you know,

how, how are you thinking about initial launch strategy?

You know, where are these ATD patients typically treated? Are they concentrated in centers of excellence or do you need a community referral program or are they all of the above? How are you starting to think about, you know, actually targeting this in a commercial way?

Yeah, it's not too early at all. I think we actually think about this a lot. So there's, you know, probably at least 100,000 patients in the U.S. are ZZ genotype. That's our target population. Of those, we know about 10,000 to 15,000 are diagnosed. Okay, so it's a largely underdiagnosed disease still. And of the 10,000 to 15,000, maybe 9,000 are on augmentation, something like that. So the large majority are taking therapy, but everyone's pretty educated about their disease if they've got the diagnosis. So that's your initial addressable market, right? And that launch will be primarily through the academic key opinion leaders the ATD treatment centers you know these are these are specialists right this is still a rare disease and that's clearly a very biotech friendly kind of launch we know these folks we're working with them now they're they're partners with us um so we feel quite capable of of um of moving there and that's a large addressable market right if you think about 10 to 15,000 patients at gene therapy pricing um from there though you know we're not done yet right so we then have to think about how do you find the other 85 to 90 000 patients who are not yet diagnosed now some of them may be zz but not yet symptomatic right and that that that would be a group that we'd want to find and treat before they get the disease right um but many are symptomatic uh but they've just not completed the diagnostic odyssey you know so they may be living in a respiratory clinic they have copd diagnosis they may just be primary care and be complaining about fatigue you know um there's there's an awful lot of that out there and so that is more of a diagnostic campaign that would happen over the subsequent years i think of the analogy to like a ttrcm right where you have to go you have to go find those patients educate them you know get them to the right centers and then you can treat

got it okay that makes sense and that's a really large opportunity if you can improve those diagnosis rates over time, a la ATTR. Yes.

Okay. And so you have alignment with the FDA on your path to accelerated approval. I'm just wondering if you could just walk through your engagement with FDA thus far and overall regulatory strategy and thoughts on the confirmatory study as well.

Yeah. FDA has been great. I know it's been turbulent over there and investors have had a lot of questions, but I always remind people that the commission is not our reviewer. We have had actually a lot of consistency in our reviewers over the last several years in these programs. That's true for sickle cell and for alpha one. And I think by and large, as I have always experienced, I think the FDA really, if you bring them really good science and really good medicine, they are very eager to help and do it in a thoughtful way. You just have to find the way to help them satisfy their demands, which is they have a lot of statutes they have to live up to, and that's good. So they've been great. So they've been working closely with us for years now. I think it's an example of that. We got RMAT designation, which is sort of the breakthrough therapy for advanced therapies. We have this CMC program called CDRP, where we get also extra advice from them. I think they're clearly understanding that base editing is a very frontier kind of technology, and so they need to be very proactive with us to help us understand how to get it ready for filing. And that's been incredibly helpful. And then, as you noted, we're now in an accelerated approval pathway. And that, of course, relies on their guidance to say, you know, yes, this could make sense. And we align with them on that path. And again, I think, you know, this is not a big stretch to see this as an accelerated approval candidate. You know, accelerated approval is an approved statute for the FDA to use when you have enough biomarkers and science to suggest you are likely to have clinical benefit, which can then be confirmed in a confirmatory trial. Well, here, you know, we have any number of biomarkers all pointing the right direction, all exceeding the threshold that would say this person should no longer have the disease. So I think it's a very clear candidate for that. So I don't feel like we got a special favor. I think it was actually kind of right down the middle. Then we will have to come back, and we are doing so to design the confirmatory trial, which will help them establish the functional outcomes that they will want to see in coming years, and that'll be the next step of the process.

Before I move on to the rest of the pipeline, is there anything else AATD-related that you think is important to really highlight?

It's a great question. I mean, I think mostly just to step back and kind of remember, like, what's going on here. I mean, This is the first time, as far as we know in history, that we have a drug that can not just intervene genetically, which has been kind of the new wave of medicine, but literally rewrite a sequence of the genome back to normal. You know, it's a profound event, and I think it's gotten a lot of interest. And so as excited as I am about ATD, I'm equally, maybe it's a good segue, equally excited about that paradigm and our ability to now use what is effectively a platform technology to now march through mutation to mutation, always in this case, maybe the same organ using the same delivery technology, the same editing technology to increasingly predictably and reliably make these same kinds of interventions for more patients. So I think we're opening a door here to a whole new kind of medicine, which is very exciting.

It is a good segue, because next I want to spend a little bit of time on PKU, and particularly, you know, what you're alluding to is that, you know, FDA sort of pathway or platform multi-mutation sort of IND, essentially. So maybe talk a little bit about the PKU opportunity. You're nearing your phase one, two initiation later this year. And just frame a little bit how you're leveraging that regulatory flexibility, specifically for here, and then maybe even expand it beyond in your plans for additional indications. Yeah.

So, so, you know, you'd asked before about regulators, you know, so this, this is an example where the science makes something possible and the regulators are following that science, right? So, so with, with LNP delivery, right, we have a synthetic, highly predictable delivery vehicle and we have an RNA payload and if, of a certain LNP, if we run the preclinical talks again and again and again, even when we're changing the order of the letters of the RNA, it doesn't change the acute talks, right? it's always the same so it's highly predictable and repeatable and then for the payload the base editor again you know we can change the guide rna around you'll have different on and off target edits so you have to check those of course but the acute talks the manufacturing it's all going to be identical right so that's a true platform that that allows us to to with you know have high confidence every time we do it you know the next time and so this so beginning under peter marks actually in the prior administration uh he was really at the forefront of saying wow okay this should enable a different kind of medicine right we should be able as regulators to sort of see one set of studies with one one editor let's say and once it looks good we should give you credit for that you shouldn't have to repeat all those studies every time uh and in fact even more than that you should be able to say you know i'm going to make the same genetic change but just a different mutation, you know, but that should live under the same program, right, every time. And so this was sort of very forward looking of Peter to start laying this out. But then, you know, some of the best ideas in government are the ones that survive administration change, you know, then we're now in the Trump administration, Dr. Macri comes in, and he says, this is amazing. Now let's take this to the next level and talk about plausible mechanism pathway, which is exactly this point, which is we know that if I'm fixing the PKU, the PAH gene, and I'm correcting a mutation that's causing high phenylalanine, it doesn't matter which exact point mutation I fixed, it's going to have the same effect. And therefore, if you show me once or show me twice that it works, the third, fourth, fifth time, I'm going to give you credit that you can just build on that same foundation. And that's where we're living now. So very, very exciting new world. So as you noted, We have an open IND for BIM304. This is to correct point mutations in the PKU gene, PAH. We would expect, you know, again, as with alpha-1, that a single dose ought to be able to fix enough enzyme that you can then metabolize phenylalanine normally and hopefully get patients towards a functional cure. And then this IND already has two different editors in it, right, treating two different mutations. They'll be slightly different patient populations, but all mixed up into one trial. And then as we qualify and bring forward new editors, we will then add number three, number four, number five, some of that in development, some of it on the commercial market. And again, it's a very new paradigm, so we're going to learn about this together with the FDA, but it's very much right down the middle of what they were trying to outline with the plausible mechanism pathway guidance.

When you bring a new mutation onto the market, let's say you're already approved with those first two, how does that work? Do you have to do just a very short study? Do you not have to do a study at all?

So we'll see. In theory, if you really read their guidance, it may not need clinical trial at all. You know, I mean, I think we'll have to see. But what you, I'm sure, will have to do is you will need to show some amount of potency information, may or may not involve more animal studies even, right, but at least in vitro, you know, possibly in vivo, and then in vitro off-target asset. you'll have to sort of make sure you've shown for this specific guide here's the off target pattern and everybody's comfortable with that and then you move forward um but you know the whole point is to avoid having to redo clinical trials right and and in fact if you think about it in the limit where this is going is ultimately individualized editors right that's the that's the end game we call that n of one and we've already seen that with baby kj that the chop team in Pennsylvania did. There, by definition, you can't do a clinical trial on the commercial market because you would have treated the patient. There's no one left to treat. It's a unique mutation. So I think in theory, this system is designed to not need the clinical testing every time. So long as you have a plausible mechanism for the effects should be the same every time, and you're seeing consistent effects, I think then the FDA will give you that runway and latitude.

Yeah, no, that's really exciting. Excited to follow that as you progress it. But maybe just to go back to PKU as an indication you've selected, you know, what makes it ideal for a base editor to come in, you know, outside that there's multiple mutations that you can target?

Yeah, it's a, you know, it's a high-end need disease. Patients are generally not controlled, despite available therapy. It is an extremely life-disrupting disease. You really can't eat normal foods. There's all sorts of social impacts of that. And in the many ways in which you are generally uncontrolled, it modifies your executive function and cognitive ability, sometimes, you know, very deeply. um and so it's a it's a really tough disease there are some products that work okay for some patients you know you've had these bh4 cofactor types of products um huvan now cefiance maybe has a little bit more of an impact but still you have dietary restrictions you know it's not getting that all the way to a to a functional cure we've tried gene therapies they generally didn't work you know av has been a tough tough platform uh to see that come through so at the end of the day i I think a one-time LNP containing a base editor, if we can fix enough of the enzyme, we ought to be able to open up the spigot and start the flux metabolizing phenylalanine and just drain it out of the body no matter what you've eaten. I mean, that's basically the concept, and that would be a one-time durable effect.

Big change for those patients. We're running out of time, so I want to make sure that we talk a little bit about sickle cell because you are nearing that BLI filing. and I do, you know, even with me, it feels like it can be overlooked sometimes. So how are you preparing for commercialization? How should we think about that early launch? We've learned a lot from CasGebby, but what can you do to really drive perhaps even a more successful launch than CasGebby?

Yeah, great question. I'm going to have Shrevan cover this one.

First of all, thank you for asking the question. We always appreciate the focus on risk to sell. I'd say a couple things. One, and it would be remiss to not acknowledge it. We just hired a new chief commercial officer, Eric Foster, who just joined us from Art Deluxe. Really excited. Lots of experience in rare disease. I would say from an overall organization perspective, we're very focused on the launch. It's a whole student body effort right to make sure this happens, whether that's building systems, processes, you know coming up with plans in terms of manufacturing from a capacity perspective and a quality perspective so every part of the operations aspect of the company is very much gearing up for the launch and so that's the the back end I think on the front end I think we've increased the presence that we have from a medical perspective and and from a field perspective and I think that ramp will continue into next year as we get closer. Operationally, also, we're very much focused on submitting our BLA as early as the end of this year. Maybe it slips a little bit into the early of next year, but as early as the end of this year with, you know, hopefully a quick review and launch. And I guess just from a total market opportunity, I guess, how should we think about that? just given what we know on the slow cash chevy launch you have a lot of differentiation um in various parts of the process but but how should we be thinking about what that actually looks like in terms of revenue yeah i don't i don't think our views on this have necessarily changed we think still think this has a blockbuster potential as a whole and from a peak sales perspective for beam um you know our cuts for the patient population that uh risk to sell can treat already assumes some amount of selection. There's 100,000 patients that we think in the United States with sickle cell disease. We think about 10,000 patients are about the right patient population size for risk to sell. And that assumes these are the people that are willing to step through conditioning to get there. With respect to the competition, it's not just Caschevi, it's Lifgenia. But I think what we've seen is we're coming in and being the third to market here. We get the opportunity to learn from their approach. We also get to ride some of their hard work in terms of seeding the market, whether it's working with hospital systems to build contracts and sign contracts, you know, processes within the systems themselves. Some of those things are now, the hospital systems across the country all have familiarity with this therapy, at least the ones that do treat the sickle cell patients and the ones we'd start out by, you know, marketing to. So I think that from our perspective, we see the potential there. We think our differentiation will carry the day, whether that's our ability to get to a 60-40, you know, fetal hemoglobin to sickle ratio, our resolution of anemia, our total, you know, time to engraftment being, you know, about two weeks, 16 and a half days. Just overall, I think we feel really good about what we have and we think we have a potential for real class preference.

Yeah, looking forward to that. And you've also prioritized in vivo as your next approach in sickle cell disease recently. So I'm just wondering if there's an update or you could share just where that program stands, like how close to moving this into the clinic as a quick follow on for risk to sell is the company?

Yeah, look, I think we wouldn't have made the decision we did or announced at the start of the year, if we didn't feel confident that we have a path forward, I think we're in the process of making sure we have it right before we nominate it as a drug candidate. And when we do feel like we're there, we'll come back to the market and share. But I mean, I think it's at some point, stay tuned is my response.

I'll work on my patience. Okay. All right. Well, I think we've covered a lot here. Maybe just turn it back to you, John, for any closing remarks that you might have and to recap the runway and just, you know, the positioning that BEAM has over the next 12 months.

Yeah. So it's been a great discussion. I think we've covered a lot. You know, I'd maybe add to the near term that we will also have first in human data for another metabolic disorder, GSD1A, again, fixing a mutation here, RD3C, that's BEAM301. That'll be a couple of cohorts of data um and that'll be this year um you know their ultragenix had a recent approval looking at cornstarch reduction that's a that's an okay end point we also think about time to hypoglycemia so um so i think that's a near-term point long-term you know i think we have runway into mid-29 you know we're well financed uh we will have a commercial sickle product by then we you know i think alpha one will be right around the market uh you know around that time we haven't tighten that up yet, but we'll do so in the future. Uh, if you think about the speed with which we can get sickle launched, then an alpha one accelerated approval, you know, PKU is pretty fast too. You know, I mean, it's obviously the clinics it'll be behind those, but not far behind, you know, it's a pretty efficient development process. So, so we think all three of those are blockbuster potential franchises where we can make, you know, gene editing into a real business and become a sustainable multi-product company. And all of that is using this same platform that is now built. And as we talked about a little bit along the way, I think the opportunity to now exploit that platform and target it now at many other diseases and continue to grow on that base is just what's so exciting for us on the long term.

Well, lots to look forward to there. So thank you so much, John and Travman, for the time. This has been wonderful, and I really appreciate it.

Thank you.