BridgeBio Pharma, Inc. (BBIO) Earnings Call Transcript & Summary

Okay. Good afternoon. We'll continue with the next session. I'm Paul Choi, and I cover the SMID cap biotechnology sector here at the firm. It's my pleasure to welcome BridgeBio to the session. And joining us here on stage is Neil Kumar, CEO. What we'll do maybe is let Neil kick it off maybe with some introductory remarks, maybe just on the portfolio and the approach and the model, and then we'll get to Q&A after -- a deeper Q&A after that. If there are any questions in the audience along the way, please raise your hand, and we'll try and get a microphone to you.

But otherwise, maybe Neil to kick it off, Bridge is a multilayered story with a pretty broad and deep portfolio. So maybe a question one to you to kick it off is just how do you think about managing all this and just sort of rationalizing a strategy that accounts for all this complexity?

Yes. Thanks, first of all, Paul, for having us here. I know it's late in the day and late in the conference, but we've appreciated the opportunity to present and the box launch and the great weather you provided. Maybe I'll start with some comments on how we think about problem solving. And I know you and I have talked about this over the course of years. But I kind of almost wanted to go back 20 years in my career to when Brian, our CFO, and I were in graduate school. And actually, we happened on a lecture that was occurring in the Department of Physics at MIT, but it was really on religion. And the purpose of the lecture really was to ask the question how ought you approach a religious stance if you don't believe in a conscious God, this is going somewhere. And the theory and the case back then was, one should be an agnostic because you can't concretely disprove the existence of conscious god. And the lecture was pointing out that, that actually isn't necessarily consistent with a Bayesian mentality. But rather one should look at the preponderance of evidence, and the first person who offered this theory up was Richard Feynman, that if the preponderance of evidence in his mind and his colleagues minds, I guess, suggested that there was no conscious god, then it is purely rational to be an atheist. And I was -- I wrote down his quote. He says every one of the concepts in science and religion is on a scale graduated somewhere between, but at neither end of absolute falsity nor absolute truth. And so I was thinking about that, that's obviously a Bayesian way of thinking, right? And that is what we try to do in everything that we sort of think about at Bridge, both in bringing new programs in or in terms of evaluating our ongoing programs. And what do I mean by that? I mean that there is really no capital T truth in biology, right? There's no physical law. You can't write down a closed-form set of equations that describe how when you swallow a pill, it transits the gut, and it binds to a certain target and ultimately produces a certain functional outcome. But what you can do is add up information at different levels from the molecular level to the cellular level, to tissue level and ultimately, to clinical presentation. And I think we've sort of gotten away from that as an industry, in part because of the hyper-specialization that we see like my statistician who may be a frequentist thinker doesn't really know cellular data that well and so therefore, may not trust it. He'll only trust in RCT, and it may also be because of the hyperproliferation of information as well. But I'm speaking about all this in the Bayesian approach because I've been asked the same question over and over today, which is, is infigratinib, more efficacious than vosoritide. And I'm sure you'll ask that as well. And one of the things I think about is we could talk about a point estimate that we measured in a Phase II trial, but I'd like to go back to the fundamentals of what's known about the disease, right? At a molecular level, we know that it's FGFR3 gain of function. We know that gain of function turns on 2 effector pathways, right? And so we hit both effector pathways, vosoritide hits one of the effector pathways. Okay. Now you go to the preclinical cellular models that look at chondrocyte differentiation and proliferation, which are the abnormalities in this condition. And what we find is that infigratinib outperforms vosoritide in terms of correcting the dysregulation. Then you look at the preclinical animal models and you find that infigratinib outperforms vosoritide. Then you look inside the clinical data, and you see that every point estimate suggests a greater degree of magnitude on change from baseline for AHV across various time points. You see that it's a higher responder rate. You see that the impact on proportionality is greater and statistically significant, et cetera, et cetera, et cetera. So then if you add all that up, you say, my prior suggests that one drug is better than the other, even though I haven't run a double-blind head-to-head, right? Similarly, someone asked me this morning, they said, well, how do you know definitively that acoramidis is a better stabilizer than tafamidis? Well, I don't know anything definitively. That's the point, right? There's no capital T truth is what I just said. But what I can do is, again, start at a molecular level and know that it's a superior binder, better KD2. That is delta GU superior, it does a better job of glueing the tetramer together. It's consistent with the structure of the compound, that ultimately, what we know about it is it has a better free fraction, so it sees more target. That in 4 of 4 clinical assays that were published prior to some recent assays, we see that as a superior stabilizer preclinically that we see in the clinic in intertrial comparisons that promote serum TTR to higher levels than tafamidis, and that patients on tafamidis when they go on acoramidis increased their serum TTR levels some 35%. And so how do you weigh all of that evidence versus one Flag-tag E. coli derived assay where the probe is not actually displacing acoramidis. I think, again, you have to go back to your Bayesian thinking and say, I ought to believe that acoramidis is a better stabilizer than tafamids unless I weight this data point over those other 14, and that's not really consistent with that Bayesian approach. So that is really how we approach thinking inside of BridgeBio, knowing that capital T Truth cannot be arrived at very easily.

So I think a lot of investors who follow you probably were assuming they need to follow cell biology and statistics, maybe weren't as aware that they'd have to follow their humanity classes again and Holmer and Richard Feynman in terms of philosophy. So you've given us a lot here to discuss and maybe just starting with each of the programs here. Most recently, as you mentioned, you talked about infigratinib. You've released Cohort 5 top line data, and the discussions I've had with investors in recent -- since you guys have disclosed that updated data is just maybe understanding how we should approach looking at the data from a Phase II study without a placebo controlled, understanding what is like-for-like on a Phase II versus another Phase II or versus the Phase III on label data there as well? And then maybe, secondly, frequent comment I've gotten in my investor discussions is how do you account for age, sex, racial differences here? And just basically, how do we understand this on an apples-to-apples basis. So maybe walk us through that.

Yes, it's a great question. So I mean, I've written some of the stuff down just so I make sure I get the numbers just right. The 2.51 centimeter per year at 12 months and 2.5 centimeter per year at 18-month data that we posted as it relates to achondroplasia represent a 60% improvement as compared to prior Phase II Acorn trial results. And as you know, we showed the first and only statistically significant change of proportionality with a change of 0.12 -- negative 0.12 at 18 months. And I think we've published on a slide how that compares to either Phase II data that have come before us or Phase III data where it actually looks even better since you saw some slide from Phase II to Phase III in the BioMarin data, but all well below [ 2 ]. So this continues to be, obviously, the most efficacious product that we've seen, again, very consistent with everything we know from cellular modeling. And I think in terms of baselining these things, you asked about gender. I think the gender baselines were basically the same 60% female, 40% male. Actually, age should have benefited them not us, because what they show is in these different age ranges, 5 to 8 and 8 to 11, you actually do better in 8 to 11 and we have a slightly younger population, 7.25 years versus their 8. So that should have actually biased against us. And then I think someone was helpful enough to send out kind of a rebaselining that they had done, very interesting. I think their cutoff was chosen basically simply because they were able to overweight some of their super responders, which isn't really like the way you're supposed to cut data, right? These are small ends anyway. So -- for instance, the 4 patients that they have when they cut their baseline by 3.5 or less, they're all well below 2.5. And if you cut it at 3, like our point estimate is numerically way superior to theirs. So this is all kind of arbitrary, I'd say, at the end of the day, these are small ends. It's pretty clear that our drug is providing greater efficacy in terms of absolute AHV, in terms of change from baseline AHV, in terms of responders, the number of kids that are actually responding. I think you see that at 6 months, 12 months, 18 months as the standard deviation and standard error come down. And I think most importantly for us, that really starts to give us a lot of confidence in the Phase III clinical trial, which was powered for 1.35, then we powered it very conservatively to be like BioMarin but I think it will be a substantially better product.

Okay. Great. Maybe just a couple of follow-ups on that in terms of -- you touched on it a little bit, but just how do you think about -- since we haven't seen patient level numbers the way you presented it with the earlier cut of the data, just maybe outliers and/or super responders and age-driven sort of natural growth potentially affecting the mean or the point estimate. And then, I guess, as you think about your Phase III program, just sort of what you can say in terms of the enrollment status. You said you mentioned it -- you've powered it very conservatively. The Phase II data suggests to date that you have a pretty wide margin of error here, so to speak, in terms of hitting stat sign on the Phase III trial design. So maybe touching on those points.

Yes. So on individual data, we actually did publish the dot plots very consistent with what the New England Journal figure was in the vosoritide paper, and we'll continue to elaborate on all that data when we publish it. But what you can see is that the data set was not driven by like a single or two [indiscernible] I mean, you can look at it and the clustering becomes tighter as you go out over time. That's why I really like the 2.5 and 2.5. I'd say additionally, what is true is that you have a lot of responders, right? So it's not [indiscernible] materially different than what's been seen before and pretty consistent with what we saw in our 6-month data as well. So in terms of enrollment, enrollment is actually going quite well. We didn't feel the need to release this data because of anything in and around enrollment. I think we'll have the opportunity to overenroll this trial if we want to. And again, we continue to guide to enrollment this year and read out next year.

Okay. Just maybe something you mentioned briefly, just on the publication strategy, you've talked about that coming at some point. Maybe can you just sort of update us on the status of that when that might potentially come...

Yes, we're submitting it -- writing it up, and we will submit it to a journal. So I expect it will get published sometime this year.

This year. Okay. Great. Maybe one more to close the discussion on infigratinib and in the Acorn program is relating to sort of the regulatory landscape. You're thinking -- you've talked about your time lines for completing enrollment of the trial when data -- pivotal or top line data might potentially come. But I guess the question we get is thinking about BioMarin potentially getting a full approval for "Voxzogo" closing the loop on that? And just sort of what -- how do you think about that? What does it mean from a regulatory review for you guys and just any perspective there?

Yes. I don't think it means anything for regulatory review on our side given our EOP2 meeting. So I still expect to be able to run our 1-year trial as we've suggested. For their full approval, I don't know what their regulatory discussions have been. So I can't comment exactly on what the -- how long that would take to get the full all the way through growth plate closure. I don't know how many years they need.

Okay. So your view is that 52-week data here based on your end of Phase II discussion is sufficient versus longer term like?

Yes, definitely.

Okay. Great. Maybe moving on to ATTR. And starting with your most recent data set there as well, you presented a series of really interesting regular data update on acoramidis, including at ISA. Can you maybe just review for us what the sort of key data you presented there was? And I also want to dig into some of the academic studies that came out of that meeting as well, too.

Yes. I mean ISA was super exciting as always. For those of you that don't know, it's probably the most important amyloid conference that occurs once every 2 years, actually occurred this year in my hometown in Rochester, Minnesota, and we had 12 posters there. I think that the most exciting for me, quite [indiscernible] my posters are same. But the most exciting for me was tying serum TTR elevation numerically to decreases in mortality and to decreases in cardiovascular hospitalization. As you recall, going all the way back to Eidos days, the question was always, okay, yes, acoramidis may be a better stabilizer than tafamidis, but how much does that added stabilization actually get you in terms of functional benefit. And we have seen some studies out of BU in the variant population tying ever higher levels of stabilization as measured by serum TTR levels to ever better outcomes. But this was the first time we were able to publish on ever higher levels of serum TTR in the wild-type population, tying to levels of mortality and hospitalization. So ultimately connected dots between stabilization and [indiscernible] for the patients and physicians that we serve. I think there's a bunch of other exciting posters that we put up, but maybe one of the more exciting posters that came out from Dr. Maurer's, yes, exactly. So there's one in and around tafamidis plus knockdown, but there was another on acoramidis and tafamidis. And what was very heartening there is you see the outperformance of acoramidis similar to what Dr. Masri published at HFSA and then again, elaborated on at ISA. But I think the other big one was what you were able to see was 100% survival quite a long ways with acoramidis consistent with our Phase III in Japan. So the absolute levels of survival that are achievable now if you catch your patients early enough and treat them at these elite centers is really remarkable considering where we started just 5 years ago, right? So that was all pretty exciting.

Cool. So maybe let's talk about the company data sets separate from the academic data sets. And I guess, first, remind us was this analysis of serum TTR and the clinical outcomes preplanned? Or was this backward look in terms of data crunching? And then secondly, what does this potentially mean for your regulatory prospects here? Is this something that you're thinking about as potentially being inclusive on label and just maybe frame the situation there?

I think stabilization in serum TTR levels will be in the label that's consistent with what [indiscernible] tafamidis as well. So that's my full expectation. Yes. I think these are all planned analyses. One of the things that, I think we've talked about is our hope or goal was to publish at least 25 substudies coming out of ATTRibute within the first 18 months post the top line. And I think we're well on our way to doing that or beating that. You saw the CMR absolute reversal of amyloidotic plaque in the heart that came in the conference before or 2 conferences before. The last conference, the ESC heart failure, you saw that we presented within our entire 632 population that we hit stat sig on ACM when you include the sick patients so that you can up the event rate. So we continue to publish on various subpopulations an exploratory analysis.

Okay. Great. One more, I guess, just in terms of the company-specific data sets and additional analysis there. Just maybe remind us what other data sets you'll publish here. And obviously, your PDUFA in the U.S. is coming up here in November of this year. And so just maybe just sort of what other updates you will expect from the program outside of the regulatory updates?

Yes. I think you can continue to see us try to connect the dots between ever better serum TTR and ever better biomarker or a functional response from the NT-Pro level and some of the other biomarkers that you can look at troponin and then ultimately functional outcomes. So expand that into quality of life, et cetera. So that's one piece of it. The second is we'll have 1 year OLE follow-up right before the PDUFA. So I'm excited to have a look at that data and publish on it. And I think the opportunity will be right around ESC or somewhere right after that. I can't remember exactly which conference it will be so that should be exciting as well. Those, I think, are the two big buckets of publication. There's some other stuff just around disease awareness, AI approaches in terms of diagnosing and things of that nature that we're working on. So it should all be of interest.

Great. I want to pick your brain just on one science question, which is this is something that's starting to go around a little bit in investor circles, which is there are certain classes of drugs, statins, ACE, ARBs and so forth that are called -- characterized as cardioprotective by ESC and ACC and so forth. I guess, just based on the serum data that you've seen and the correlation with clinical outcomes, is there a view here that acoramidis is cardioprotective, and just is there, I guess, support from a guideline perspective that this could be viewed as a cardioprotective mechanism?

Yes. So it's a very interesting question. The -- I think our ACT-EARLY trial, which is our primary prevention trial, if you will, we'll ask and answer some of those key questions. But if you go all the way back to, there was a Scandinavian study done, maybe a decade ago now that looked across tens of thousands of patients and asked whether or not people with higher levels of serum TTR had fewer downstream cardiovascular events and actually less mortality, and it turned out that higher levels of serum TTR are correlated with less frequency of heart disease and actually a longevity. So yes, I think there's a really interesting thesis to be put forward there, but we need to prove it with more clinical data.

Okay. Correct. I want to turn maybe to one of the academic posters that was presented there out of Columbia University, at Dr. Maurer's Group, which analyzed the combination use of tafamidis and ATTR silencer that basically showed no -- little-to-no difference versus tafamidis monotherapy. Now I want to caveat to the statement by saying it was a relatively small study, single center, and it was backwards looking as well, but it was kind of an interesting analysis. And so I guess, from your perspective, Neil, how should we interpret the study given the caveat that I just laid out? And what does this, I guess, implicate for stabilizer/silencer combination therapy potentially here?

Yes, it's hard to know, again, I mean, let's just -- let's take the Bayesian prior approach for a moment. I mean we didn't see combination being all that effective in APOLLO-B against the primary endpoint of 6-minute walk. And here, again, we don't see there being a lot of differential effect, caveat both of those by saying the ends are relatively small. From a biochemical standpoint...

For APOLLO B and this particular study...

Yes, that's right. If we go back to biochemical standpoint, I think there can be a case made for a partial stabilizer benefiting from a knockdown and/or an incomplete knockdown, benefiting from a stabilizer, for instance, with Alnylam, our belief is the mean max knockdown of 84% or so. If you come in with a 60% stabilizer as is tafamidis, where you're taking those 16 remaining toxic monomers and let's say, you're stabilizing around half. Might there still be functional benefit from that? There might, and I think we'll probably have a better answer to the question post HELIOS-B, just given the population that will be on top of there. So I thought it was intriguing data that Dr. Maurer -- as always, he's a very careful investigator. But I think we'll learn a lot more from HELIOS-B on the topic.

Okay. Great. I just want to take a pause. If there are any questions in the audience, please feel free to raise your hand, and we'll get a mic to you. Just look around the room for a second here. Maybe in the meantime, as we just mentioned -- discussed here a moment ago, you have an upcoming PDUFA for acoramidis in November. And so I guess, sort of what updates between now and then do you plan to provide just on your regulatory interactions in terms of checking the box items and things like that? And then secondly, relative to the Vyndaqel and Vyndamax label, I guess, in your mind, what does sort of a best case label look like for acoramidis?

Yes, it's a good question. I mean, I don't think we had planned on making any formal announcement in and around the interactions with the agency, but I can say they've been positive. We had our mid-cycle review meeting, everything remains on track. As you know, the clinical data is clean. This is not a complicated molecule to synthesize and I think our clinical trial inspections have gone fine. So all of it remains on track from that standpoint. Labeling discussions will begin late this summer. So I mean we've already had a little bit of back and forth on it. So I won't know until the bolus of those comments come. And I think the thing that to look for in the label is obviously those absolute levels of survival, hospitalization, the early separation that we have. And then how does that play into the various levels of improvement that one sees in our trial [indiscernible] what you saw in ATTR-ACT. Those are the key elements. I think many of them will get into label.

Okay. Great. Maybe turning to the commercial piece because you'll be in a position to launch potentially by late end of this year. Can you maybe just update us on how your commercial build-out is progressing? What are sort of the pieces that are outstanding, whether it's key hires, payer discussions, things like that?

Yes. So I mean maybe we start with the MSL force, which is fully hired now and out there, and now we're getting them straight, to really speak, as broadly as they can on the attributes of acoramidis. As you know, we're in this sort of pre-promotion phase, so we have to be very careful right now about what we do. We've hired the totality of our senior sales force leadership. And actually, we've had a lot of really great interest from a lot of very capable folks on that front. We do -- and as you know, we are able to talk -- call on payers now, and we have been doing that. So we've been having substantive discussions on that front. We've also had substantive discussions on the LDN front, both with SPs and SDs. So we'll be narrowing down our network there and then on the hub side as well. So we're feeling pretty good about where we are in terms of overall commercial buildup with the aim to be ready to launch beginning of November, should we get a little bit early.

Great. Maybe just on the label specifics aside, as you think about the commercial strategy post launch, maybe the #1 thing we hear from doctors is just cost burden for the patients in terms of affordability of tafamidis currently. A lot of these dynamics will change over the near-to-intermediate term with IRA and changes in the catastrophic cost equation. And so maybe just can you frame for us how you envision that landscape evolving when the out-of-pocket cost becomes a little bit normal for patients and a little bit more manageable. And just what does that mean for your competitive positioning outside of the data?

Yes. Well, competitive positioning, we continue to believe that stabilizers will be used frontline, and we want to establish ourselves as the stabilizer of choice for physicians. As it pertains to price and affordability, you can already see some of the changes or sort of like [indiscernible] next year with a blended $2,000-or-so co-pay through 12 months. This year, it's a bullet, $3,000 payment. But even with the 7% price increase that was taken by tafamidis and in addition, the lowering of the federal poverty limit, free drug coverage. You can see, I think, an additional, something like 4,000 or 5,000 patients that ultimately have come on brand and you see that reflected in their U.S. sales. So I do think affordability is taking a meaningful step in the right direction for patients based on the copay limitations associated with the IRA and it will take another big step next year.

Okay. I want to talk a little bit about the longer-term commercial outlook. Pfizer's growth, I think, in the most recent quarter was something approaching almost 100% in the U.S. year-over-year, really big number and so does the sales in terms of the importance of that franchise in terms of their top 5, top 10 products has clearly been established, and the growth is quite significant in the U.S. as patients get identified and on therapy even when you remove the price equation, price factor. And so as you think about the longer-term size of this market, we see consensus estimates pretty big for the silencer class but the stabilizer class definitely looks smaller here. Maybe can you think about -- walk us through what are the considerations, first, on the IP front? And then just as you think about the class shares over the longer term, call it, 5, 10 years out, how is the Street thinking about it or consensus estimates versus how you guys are thinking about it?

Sure. Yes. Maybe I'll start with -- I mean I think the last I looked, as you and I were discussing maybe 1.5 months ago, the consensus for us is 8% of the market, and the consensus for Alnylam's product is 60%. 8% in the second mover would be -- that would be outside of the standard deviation to the low. Typically, you only see that when someone gets a black box warning or something like that. So I anticipate us obviously being able to beat that expectation fairly handily. Again, I do think that small molecule stabilizer will be frontline and it will be a choice between us and tafamidis and our hope is that people will choose acoramidis. And I think also for those who aren't tolerating acoramidis in terms of either they are contraindicated because they are on CRESTOR or they're obviously not well managed based on their NT-proBNP or serum TTR levels, we would get those switchers. How ultimately the share evolves will depend on the 42% relative risk reduction that we put up at 30 months and separation at 3 months. If Alnylam's product or the Ionis product handily beat that at 30 months or separate earlier than 3 months, I think then there's a case to be made that they might jump to the front line. But I think if they don't, they would be second line. And if it's about the same, which I evaluate their product, it's slightly less biochemically potent than ours, I do think the orals would continue to be a first line. And the second thing is beating tafamidis everywhere in their trial, right? So as we've discussed, our product beat tafamidis where we can look from a point estimate, trends in favor of acoramidis, again, trial was -- that's post-hoc exploratory. The trial was not designed to be double-blind, head to head. So I think we're going to need to, and we will do those intertrial comparisons in the context of HELIOS-B. So that's going to determine a bit of how the share shakes out. And then on the IP front. As best as we can tell, obviously, Pfizer just filed for a new tablet formulation that will protect them out to 2041. We believe in the validity of their Vyndamax patent franchise, which has already been successfully defended in Europe, and I think it will again in the U.S. in 2026. And the fact that generic manufacturers are looking to invalidate that 2035 estate versus the go around and manufacture of Vyndaqel suggests to me that as suspected in that liquid suspension, you are getting to low free energy form polymorph when you try to make Vyndaqel itself. So I think that there's a good possibility that their franchise is defensible out to 2035 at least.

Okay. Great. 2035. Okay. In our remaining time, I want to talk maybe about some other areas of the pipeline that get a little short trip. But I think if you talk about what's -- if you could talk about what's the nearest term outside of after acoramidis, whether it's ADH1, ribitol for limb girdle? What can we see next? And what's the next coming up in terms of pivotal data that could advance another leg to the story here?

Yes. So both Phase IIIs for limb-girdle muscular dystrophy type 2i as well as for ADH1 are set to read out next year. And I'm pretty confident just based on the way those trials have enrolled to date that we will see data next year. So maybe I'll start with ADH1. I think we had some pretty interesting data at ENDO that may not get as much attention. And it was really on 2 fronts. One is the use of Encaleret in the HP population, for which I think we would have a different composition of matter, different molecule that we might take forward. But some exciting data there, both in terms of serum and urine calcium. And then on the second side, it was the natural history study, which suggests that standard of care really isn't doing anything for these patients that's substantial. So again, if there was any doubt on probability of technical success, I feel like that's the highest probability of technical success program that we have ongoing. When we were talking to physicians, and I encourage folks who have maybe looked at this space months ago but haven't revisited it, now with the tool out there, people thinking about it. People are seeing the studies [indiscernible] nonsurgical hypopara patients are actually ADH1 patients. People are finding more and more of these folks. And when we've talked to a few of the expert centers, they say, well, this resembles to us an XLH like category. And obviously, these physicians see XLH and ADH1 patients. So obviously, the phosphatonin FGF23 antibody, that Ultragenyx has along [indiscernible] ended up being a very nice product for patients and for the companies alike. So I think the prevalence of that condition it's probably closer to the stat epi that we thought, but when we were enrolling it first, it looked a little bit smaller. So 3,500 patients identified in the U.S., stat epi suggests 10,000 to 12,000 patients, that's probably somewhere in the middle, but it's not 3,500. It's not ultra-rare.

Okay. In our remaining time, I want to talk a little bit about some of the corporate and strategy decisions with regard to capital and something that you've done in recent quarters here.

Let me just mention LGMD2I -- sorry, I didn't mean to not talk about. So we will have an update on that this summer. So we had our EOP2 meeting, and I think the trial continues to enroll quite nicely. So we'll have an update there in the next month or 2...

Okay. Great. So earlier this year, you did partner with Bayer in terms of the European rights for acoramidis. You also entered into a financing agreement with 2 investors to raise capital as well. So I want to talk a little bit about how do you think about your capital position for -- between now and the longer term becoming commercial stage? And just sort of how your financing needs stand currently versus what you'll need for commercialization and over the longer term?

Yes. I mean I think we've said publicly that we're financed well beyond end of 2026. I mean at this point, we feel like we've finished financing, and we anticipate being able to afford the launch. Obviously, we've got a big chunk of cash incoming at PDUFA, which I think that plus the revenue will fully finance the late-stage pipeline. And you've seen us take actions like spinning out BBOT. I think there are some early-stage programs that investors don't really avail of in terms of value creation, in the context of the broader Bridge where even at programs like ADH1 and LGMD2i aren't getting credit. So I think you can see from us some creative steps that we'll continue to make sure our own shareholders can gain the upside from some of those earlier programs that are at once exciting, but I don't think we'll move the stock price in the near term but we'll take up some burn. So...

Okay. Yes. Great. we're up on time here, so we're going to have to end it on that note. Thanks to Neil and BridgeBio for joining us, and we'll end the session. Thank you very much.

Thanks, Paul.