Intellia Therapeutics, Inc.

Hello, and welcome to Intelia Therapeutics' second quarter conference call. My name is Chloe, and I will be your conference operator today. Please be advised that today's call is being recorded. I would now like to turn the call over to Jason Fredette, Vice President of Investor Relations and Corporate Communications at Intelia. Please proceed.

Thank you, operator, and hello, everyone. Earlier this morning, we issued a press release outlining recent business updates in our second quarter financial results. This document can be found on the Investors and Media section of Intelia's website at inteliatx.com. At this time, I would like to take a minute to remind listeners that during this call, Intelia management may make certain forward-looking statements. We ask that you refer to our SEC filings available at sec.gov for a discussion of potential risks and uncertainties. All information presented on this call is current as of today, and Intelia undertakes no duty to update this information unless required by law. Joining me on the call are John Leonard, our chief executive officer, and Ed Dulac, our chief financial officer. With that, I'll now turn the call over to John to begin our business discussion.

Thank you, Jason, and good morning, everyone. We're excited to be speaking with you to recap the tremendous progress we made in our phase three development programs of Flamvozi in hereditary angioedema, or HAE, and Nexi in trans-thyretin amyloidosis, or ATTR. The full results of our Phase 3 HALO trial in HAE position us very well for potential approval and launch of the world's first in vivo gene editing product in the first half of next year. We also have gained important new genomic insights that further our understanding of NEXE's profile and could help position us even more favorably within a large and dynamic ATTR market. Let's begin with Lombosi. Simply put, the second quarter was a momentous period for this program. In April, we reported positive top-line results from HALO and got our rolling BLA submission underway with the FDA. This was followed by our late-breaking oral presentation at IACI and a concurrent publication in the New England Journal of Medicine, Intelia's sixth manuscript in this prestigious journal. HALO was an unequivocal success as we achieved statistical significance for the primary and all key secondary endpoints. More specifically, during the six-month primary observation period, we reported an 87% reduction in mean monthly attacks for Lombozy versus placebo. 62% of patients were entirely attack-free and therapy-free in the Lombozy arm. A 23-point improvement was observed for the Lavoisier arm in the total angioedema quality of life score from baseline. For context, a change of just six points is considered to be clinically meaningful. The New England Journal manuscript also contained compelling figures and analyses underscoring the unique value proposition that could be afforded by this one-time therapy if it's approved. For instance, patient-level data demonstrated that all patients in the Lombosi arm experienced attack rate reductions from baseline from weeks 5 to 28. In other words, every single patient received a clinical benefit, including those who are not yet fully attack-free during that six-month period. A subgroup analysis demonstrated meaningful attack rate reductions in the Lombosi arm regardless of age, sex, race, weight, geography, baseline attack rate, or prior therapy. The publication also included a figure depicting the mean number of HE attacks over time. It traced patients from when they were on prior therapies before screening through the entire efficacy evaluation period and into crossover. And it showed that mean attack rates for the longvose yarn dropped well below the prescreening attack rates by week four. Attacks continued to decline in the months that followed and approach zero in the crossover period after week 28. In the placebo arm, not surprisingly, mean attack rates didn't drop below prescreening levels until patients crossed over to Lombosi. At that point, they dropped steeply and approached zero within a few months. Also, notably, all patients who received Lombosi at baseline or in crossover remained free from long-term prophylaxis therapy as of the data cutoff. and finally, favorable safety and tolerability data were observed. The most common treatment emergent adverse events were infusion-related reactions, headache and fatigue. All treatment emergent adverse events were grade one or grade two and there were no serious adverse events observed in the Lombosi arm as of the data cutoff. These results are unsurpassed by chronic long-term prophylaxis therapies or LTPs. We believe it is clear, moreover, that they truly stand alone in the HEE space given that this is a one-time treatment. Most patients were attack-free and therapy-free for the entire six-month efficacy observation period following a single long-pollution dose. Based on our preclinical work and observations from our Phase 1-2 trial, our expectation is that this percentage will increase further over time as patients who have lived with HAE their entire lives adjust to their new normal. So what's next for us? Well, we expect to be in a position to announce the FDA's acceptance of a BLA filing for Lanvozie by the end of this year. In the meantime, our pre-commercial readiness efforts are advancing well as we prepare for a potential U.S. launch in the first half of next year. Most of these efforts are well underway, including work streams across medical engagement, payer outreach, for their work on treatment center readiness, distribution planning, and access strategy. We've completed hiring for our field medical, reimbursement, and strategic accounts teams, and they're now engaging with treatment centers around the country to ensure they are well prepared to address patient needs shortly after approval. We're also building awareness of the many burdens associated with HAE. During the second quarter, we launched haereframe.com, a disease awareness initiative designed to elevate understanding of the challenges patients face, including those related to lifelong chronic therapy. Together, these efforts reflect meaningful progress in building the infrastructure, awareness, and access pathways needed to support our planned launch. So let's turn to the progress we made with Nexi, our potential one-time treatment for patients with ATTR cardiomyopathy and polyneuropathy. We were pleased to have resolved the clinical holds on our Phase 3 trials quite rapidly earlier this year, and I'm excited to report today that we were able to resume enrollment and dosing in both trials in Q2. Investigator engagement and enthusiasm remain high, and our screening rate is rapidly increasing globally once again. ATTR is a large, growing, and highly underdiagnosed market with significant omit needs. Today, patients are predominantly served by stabilizers, silencers, or a combination of the two. About a month ago, disappointing top-line results were shared from CardioTransform, the pivotal trial of eplantersin, a TTR silencer, for patients with ATTR cardiomyopathy. Since then, there's been some debate about whether a silencer can work on top of a stabilizer. We and others believe the negative outcome is specific to eplantersin in this particular trial, and it does not speak to combination outcomes in general. We remain firm believers that combination therapy will work, but only with the right agent. This belief is based empirically on clinical evidence. First, we would point to the fact that another chronically-dosed silencer, ritrizarin, has already shown a directional benefit on top of stabilizers in a well-controlled trial. But even more importantly, we would point to what was observed in the monotherapy data for each of the chronically dosed stabilizers and silencers. If you go back and look at the readouts for approved stabilizers like tefamidus and acaramidus and approved silencers like aplentersin and fritrizorid, you'll see that patients continue to progress while they're on those therapies. Why is that? Well, we and others are convinced it's because they inadequately reduce or control TTR protein. Focusing in on the approved silencers, you'll see that mean TTR reductions for each of them are about 80%. However, the details behind that number matter. For instance, it takes many months for those silencers to achieve their 80% data of reduction. There's significant variability and TTR from patient to patient, with some achieving a 90% knockdown and many others receiving reductions of only 50 or 60%. And even within an individual patient, the knockdown fluctuates due to issues with PK and issues with dose interruptions and adherence, whether due to patient behavior or toxicity. Simply put, it appears today's silencers and stabilizers are leaving efficacy on the table and a progressive disease with high mortality like ATTR-CM every day and every microgram per milliliter of TTR counts. MEXE has demonstrated its ability to deliver an unsurpassed knockdown of TTR protein for patients in both relative and absolute terms. Our phase one data demonstrated a mean TTR reduction of 90%. While that percentage is impressive, We believe the absolute TTR reduction is even more clinically relevant. When Nexi is provided as monotherapy, mean serum TTR with less than 20 micrograms per milliliter, about one-third of the absolute level seen with the leading chronic silencer. That knockdown was achieved rapidly within one month of the infusion, and it was extremely consistent across all patients. Best of all, Patients began receiving therapeutic doses of Nexi in 2021, and as of our latest data cutoff, intrapatient TTR control was constant and was maintained across all patients following their one-time Nexi treatment. We look forward to presenting updated long-term durability data at future Congresses. We believe Nexi's distinct TTR knockdown is why disease stabilization or reversal is observed in most patients in our Phase I while our would-be competitors have observed disease progression. Additionally, the response has been consistent across patients of all New York Heart Association classes, those with either variant or wild-fed disease, and it also includes patients who have progressed on past silencers. And so, we continue to have significant confidence in our ability to show a benefit on top of typhanitis and magnitude. Additionally, unlike CardioTransform, which was a time-bound study, Magnitude's primary endpoint is strictly event-based. We've enrolled well over 650 patients in Magnitude. We've been accruing events for quite some time, and those events continued unabated through the clinical hold. While still premature for us to guide us to data timing, what it can say today is that the blinded event rate in a trial remains within the range we've projected internally. We're looking forward to reviewing the detailed Cardiotransform data later this month at ESC. And of course, we have the opportunity to consider changes that further optimize magnitudes design based on what we learn. Now let's move on to one other encouraging update we're able to share today related to Nexi. As we reported late last year, grade four liver transaminase elevations had been observed in less than 1% of patients enrolled in magnitude. These were transient, and in most cases, they resolved without any intervention. Based in part on the fact that the observations consistently occurred two to five weeks after dosing, we hypothesized they were caused by an adaptive immune response. As a result, we implemented mitigation measures to enhance monitoring for transaminase elevations and intervene if they are observed. These measures are very straightforward. and could easily be implemented in a real-world commercial setting if required. We also went further. Working with Regeneron and other external experts, we sequenced and analyzed data from over 600 patient samples across all MEXC clinical trials to date. Our goal was to understand if there were subpopulations that might be most susceptible to higher-grade transaminase elevations. This work focused on HLAs, which are proteins on the surface of cells that play a key role in regulating the immune system and helping to distinguish native and foreign peptides. This blinded analysis revealed one statistically significant finding. Patients carrying one specific HLA allele that's known as C0501 had a significantly higher rate of grade three or greater transaminase elevations than the broader population. In fact, each of the five highest elevations observed following dosing occurred in patients carrying this allele. Now, some important context on what this does and doesn't mean. Only 12% of the 600-plus samples we analyzed carry this allele, and the strong majority of CO501 positive patients did not experience severe transaminase elevations. So we continue to see the potential for a favorable benefit-risk profile even in the subgroup, particularly with the mitigation strategy that is now in place. What the finding gives us is valuable, a mechanistic explanation for a general signal we'd already flagged and a way to identify patients who are more likely to be affected before it happens. In doing so, it further increases our confidence in Nexi's ability to deliver on its long-recognized potential. So here are our next steps. We're engaging with FDA to review the findings. In the meantime, we already have updated our protocols, investigators' brochures, and informed consents to incorporate HLA typing for all patients in the phase three trials. These documents are in the process of being rolled out to regulatory authorities, IRBs, and sites globally. Following the reviews, investigators and patients will be informed about the HLA results during screening or prior to crossover so they can make more informed treatment decisions. And so to close, I'm exceedingly proud of all the team continues to accomplish here at Intelia. We're marching towards the world's first potential launch of an in vivo gene editing therapy with Launvosy. We're on track to complete enrollment magnitude two later this year. and we're demonstrating precision medicine at its finest with our HLA work on Nexi. These achievements layer on top of all the other pioneering work we've undertaken as we seek to harness the power of machine editing to deliver optimal treatment outcomes for patients with just one dose. So with that, let's now turn the call over to Ed to share some financial color.

Thank you, John, and hello, everyone. In addition to the tremendous clinical, pre-commercial, and scientific progress we made in the second quarter, we also kept the company on sound financial footing. In April, we completed an equity financing that yielded approximately $195 million in net proceeds for the company. Cash, cash equivalents, and marketable securities were $628.4 million as of June 30, We believe this cash balance will be sufficient to get us at least into 2028. Importantly, while we expect to obtain approval and launch Bombo Z in the U.S. in the first half of 2027, our cash runway guidance is conservative in that it excludes all product revenues. Collaboration revenue was $7.7 million for the second quarter of 2026, compared to $14.2 million for the prior year quarter. This change is primarily due to a reduction in revenue from Regeneron. R&D expenses were $82.6 million for the second quarter of 2026, compared to $97 million during the prior year quarter. The decrease was primarily driven by lower external costs related to LomboZ and Nexi and reduced stock-based compensation, partially offset by higher employee-related expenses due to increased headcount. Stock-based compensation expense included in R&D was $9.4 million for the second quarter of 2026. G&A expenses were $37.8 million during the second quarter of 2026 compared to $27.2 million for the prior year quarter. This increase was primarily driven by costs associated with the ongoing build-out of our commercial infrastructure, higher legal expenses, and stock-based compensation. Stock-based compensation expense included in G&A was $8.6 million for the second quarter of 2026. And finally, net loss for the second quarter of this year was $106.6 million, which compared with the $101.3 million for the prior year quarter. With that, we are ready to begin our question and answer session. Operator, would you please open the line for questions?

We will now begin the question and answer session. To ask a question, you may press star then 1 on your touch-tone phone. If you are using a speakerphone, please pick up your handset before pressing the keys. To withdraw your question, please press star then 2. Please limit yourself to one question, and if you have additional questions, you may rejoin the queue. At this time, we will pause momentarily to assemble our roster. The first question today comes from Mari Raycroft with Jefferies. Please go ahead.

Hi, good morning. Congrats on the progress and thanks for taking my question. I'll ask one on the allele finding, which is interesting. For that CO501 allele, can you talk about the implications for the 12% of patients where there could be some added risk? And is there another parameter that you could use to help fine-tune patient selection? And lastly, is there more you can share on the biologic relationship for what exactly is triggering the immune response?

Thanks, Maury, for your question. So, we think that the finding confirms our initial thinking about an adaptive immune response. As many will know, HLAs are deeply implicated in cell-mediated immunity, and this would be an important part of understanding what we saw with our early observations with timing of the immune response. So it gives us significant confidence that the mitigation measures that we put in place are appropriate and are on target for what seems to be going on. With respect to the patients that carry O501, as I said in my comments during the earlier portion of the call here, we're making that information available to all investigators and patients. There's a relationship that's significant, but many of the patients that carry O501 do not have LFT elevation. The first order of business is to make sure that if patients have that, they're aware of it, and they can discuss the elevated risk with their physicians and make a determination of what's appropriate for them. Our expectation, just based on conferring with our steering committee members and people, the experts that we've been working on this during the course of our findings, is that many of the patients may choose to self-exclude, and that's appropriate for them. but for those who believe that the state of their disease and the other opportunities available to them warrant continuing to receive the therapy and advancing the trial or making the drug available for them. As we continue to learn during the course of our trial, we discuss with the FDA these findings and any further implications, but in the meanwhile, we think that this will give enhanced confidence to the physicians and patients who are entering that they can derive the best possible outcome, all things considered.

The next question comes from Joseph Foam with TD Cowan. Please go ahead.

Hey, this is Jacob on for Joe. Thanks for taking our question. Just sticking with the HLA allele, I wanted to confirm that this was something specific to Nexi and not Lanvozi. And then also you said, I believe that it was 12% of the 600 samples that carried the allele, but only a fraction of that 12% actually had elevations. Is that correct?

Yes. In my comments, I said that across the study, there's about 12% of patients who carry the CO501. And that broadly reflects what's seen in a North American, Western European population. There will be some variance across different ethnic groups with numbers sometimes lower than that, but that's what we've observed in the study. With respect to specificity, almost certainly this would be specific to Nexy and not have any implications for Lombozy. And there's a couple reasons for that. When you think about what an HLA molecule is, it binds to a very, very specific short peptide. and we wouldn't expect those peptides to be implicated in any way with the Lombosi treatment effect. So that's further supported by the fact that, as shown in the New England Journal publication that was recently released, there's no signal in patients with Lombosi. And at this point, we think that this is just a finding that's going to be limited to Nexime.

And I'll just add one thing, John. I think there's a comment about just the vast majority of those patients that had 0501 did not experience severe transaminase elevations. So 12% of the samples do represent those that are carrying the allele, but only a small subset have had these higher grade elevations.

The next question comes from Luca Icy with RBC Capital Markets. Please go ahead.

Oh, great. Yeah, thanks so much for taking my question and congrats, obviously, on all the progress. You know, obviously, we have yet to see the full CardioTransform trial. I was looking forward to that data, European Society of Cardiology, but I think, John, you already mentioned, you know, potential to maybe optimizing your trial to maximize the probability of success. Can you just talk about what are the options that you're contemplating at this point? You know, can you enroll more patients? Can you extend the minimum follow-up longer than 18 months? I don't know. Can you limit the use of SGLT2? Like, just walk us through a big picture how you're thinking about potentially tweaking your trial. Thanks so much.

Thanks for the question, Luke. I mean, the first order of business is really understanding the data that comes from the CardioTransform study. As I said in the prepared comments, we believe, based on everything we know thus far, that the findings are likely specific to apontersin and not generally applicable to how we think about treatment of patients with TTR disease or patients with receiving combination therapy. What we think is going to be the most important information is the degree to which TTR is reduced. The variability or lack thereof, as we see in our own patients, the speed with which treatment effect is achieved, and then obviously the durability as patients go through the many, many months of observation where variability may be attributable to pharmacokinetics or interruptions for toxicity, for example. All of those elements will erode the overall treatment effect, and it's important, I think, to really understand that before we jump to conclusions about combination therapy and how best to use it. But with an understanding in hand, and we will, of course, work with experts who are deep in the data, will consider if there's anything that we need to change. We remain open-minded, we adapt as necessary, and we certainly try to learn at a prodigious rate as information becomes available. The factors that you mentioned are possible to change, but we don't start with a thesis in mind until we have a really good understanding of the data. And like You all on this call and many others were very, very anxious to see what that information is before we make any changes.

The next question comes from Salvine Richter with Goldman Sachs. Please go ahead.

Good morning. Thanks for taking my question. Can you remind us of the background stabilizer used in the study and if you expect that to change given recent cardio transform results? also on the HLAA finding. Do you see enrollment changes just given screening for HLAA? Thank you.

Thanks for the question, Sylvia. Background stabilizer use is running around 80%, which is what we projected when we set out and what we've been confirming on various data releases along the way. does not appear to be changing one way or the other. I think it reflects how stabilizers are broadly used around the world and obviously in sites where we're doing the investigation. With respect to HLA, as we talk to investigators and people who we're working with in this trial, most of them view this as confidence building in terms of how to think about patients and who to enter and potentially who to exclude should the patient or the doctor think that that's the most appropriate course of action for any particular patient. But across the board, as we've gone through the data with people who are practicing cardiologists and experts in the field, to a person, all of them have viewed this as a very, very favorable finding that enhances overall confidence. and our job now is to make that information available to those doctors and physicians in the trial and patients in the trial as quickly as possible and that's well underway.

The next question comes from Sylvan Turkin with Citizens. Please go ahead.

Good morning. Maybe can you talk a little bit about the patient gateway that you're building with HAE Reframe and kind of Is that more to get data points to you for potential later marketing, or is that to kind of push your message out around some of these endpoints where one-time treatment could be helpful? And if so, what are those? And maybe related to that, what can we see at the Bradenton Symposium data that's coming up here? Thank you so much.

Let me speak first to the symposium that you referenced. You'll remember that Across the entire HAE program, virtually every single patient at some point gets to something that resembles no attacks and no therapy. It takes some patients longer to get there than others, but virtually everybody ceases to use long-term prophylaxis, and almost all the patients no longer require on-demand therapy. They may carry it with them, but the overall utilization for these patients really plummets, which we think is exciting for the patients, for the doctors, and certainly for the payers who are supporting these patients. At the symposium, we'll go through what we think is very important information for how the drug behaves from a molecular level and how you can trace that with respect to a high molecular weight kinetogen. and that has specific reference to one particular patient who had a significant benefit from the drug but did not reach an attack-free status. And the long and short of it is the patient probably has a second process unrelated to HAE and we'll speak to that. So I think that's really exciting information that speaks to one particular patient who stood out from the vast majority of patients who have all done very, very well. With respect to the website, we're trying to make sure that people have a good understanding of what the burden of HAE really is. We typically talk about disease attacks and the efficacy and safety of drugs that they receive. But what's left out of the discussion many times is what patients have to go through just to get that and stay on their therapy. and still how HAE continues to affect their lives because for all practical purposes, they continue to suffer from the disease. So by having a better understanding of what patients need to do to get the drug on a recurring basis, sometimes requiring prior authorizations even twice in a year, we want to make sure that payers, patients and doctors have a really good understanding of what that burden is. and then when they see the profile of Lombosi, the contrast will be very, very apparent.

The next question comes from Leah Kan with Brookline Capital Markets. Please go ahead.

My question has been answered.

The next question comes from Jonathan Miller with Evercore ISI. Please go ahead.

Hello, this is Yuanyuan Ang for Zhang. Thanks for taking my question, and I would like to double-click on the allele analysis. So two questions. First, how many patients with grade 3 liver signals do not carry the allele, and are there any patients with lower grade signals that actually carry the allele? And the second question is, are you considering additional prophy for patients carrying the CO501 allele, and what are the additional risks to consider for those carriers, and any particular, like, bad and others on the cell surface that has caught your attention that may be relevant for the liver injuries. Thanks.

Yes. So thank you for the question. With respect to the full data set and the analysis, we'll release that information at the appropriate time and go through the molecular findings, the statistics that support that, et cetera. And that's not something that we're in a position to do today. You asked, are we doing something different for patients who choose to participate in a study if they're O501 positive? And at this point, the answer to that is no. We believe the mitigation measures that are put in place are entirely appropriate for a cell-mediated immune adaptive response, which now we have some increased confidence that that's exactly what's occurring in these patients with these high LFT elevations. But what we have found is that we can identify patients before the event occurs and give them the opportunity not to participate, recognizing that the likelihood of their having one of these increases is higher, substantially higher than the broader patient population. If you flip it around, I think a helpful way to think about this is for the approximately 90% of people who don't carry O501, The likelihood of a high LFT elevation is extremely low, and that is confidence building for anyone who may wonder about what the likelihood might be for them, given the general data that's been released previously. And as was stated earlier, even for the 0501s, most patients will not have the elevations, but we do know that when they do occur, these tend to be the ones that are most severe.

The next question comes from Terrence Flynn with Morgan Stanley. Please go ahead.

Great. This is Chris Ahn for Terrence, and thank you for taking our question. Maybe just double-click on the HLA genotyping finding. Just kind of looking ahead, do you expect that to be potentially on the label if approved? And then in the commercial setting, do you expect every patient to get genotyped? Thank you.

I think it's too early to say. Oftentimes, as you well know, labels reflect many of the aspects of how clinical trials are done and the data that they accumulate. But that's a bridge that we'll pass when we get to that point. I think in the meanwhile, what we're excited about and what our investigators are excited about is that this will give really good information with respect to how to focus in the best possible way the benefit-risk on those patients who can most benefit from it. So we will collect information during the screening process in this study. We don't think that it will slow down screening at all. This is a relatively straightforward process, and many of our investigators believe that this will actually pick up the pace of screening, which is already rapidly accelerating. So we are very, very excited about this finding and the very, very positive things it can do for us.

The next question comes from Miles Minter with William Blair. Please go ahead.

Hey, thanks for the question. I've been getting a few inbounds since you published in the New England Journal on Lomphosy in HAE in the supplement. You show the ALT, ASTs over time, and I think in the ASTs at like week 30 to 32 in patients that got Lomphosy first up at randomization, there's, you know, It looks pretty benign to me, but there are three patients that have kind of got an excursion outside of the reference range. Is that just variability or is there, you know, something else going on there at the latest stages? Thanks very much.

Yeah. Yes. Thanks for the question, Miles. The data is laid out in the New England Journal for anybody who wants to see it. Across the entire program, there's never been an LFT elevation greater than grade two. And of those, there are other confounding reasons to consider them. In one case, as you were referring to, this is somebody late, many, many months after receiving the drug, and this is almost certainly related to another thing that was occurring for the patient, and that's what his investigator thought. The elevation was benign. Nothing was done with respect to it, and it was low grade. For other patients that we've reported in the various stages of active clinical observation, patients either were confounded by the ongoing use of alcohol with one patient who had a grade 2 that resolved rapidly. And in a second case, again, reported in the phase 3 study here, patient had LFT elevations during the screening phase and had a grade two elevation with a concomitant viral infection. Across the board, we see no signal. There's variability, as we all know, about patients, how they live their lives. And we're very, very excited about the efficacy and the safety profile of the drug as we move towards what we hope will be BLA approval.

The next question comes from Yanen Zhu with Wells Fargo. Please go ahead.

Hi, this is Jeff Han for Yanen. Thanks for taking our questions. For the Lambo Z BLA, can you mention if the final BLA has been submitted to the FDA, and if not, which remaining modules need to be completed? And based on your conversations with clinical sites for Lambo Z, are you expecting a bolus of patients at launch if approved? Thanks.

Far into the BLA filing, and I would anticipate that the next time you'll hear from us, we'll be announcing what we hope will be the acceptance of the BLA. And with that, we'll all gain a lot more information with respect to PDUFA dates, priority review, and things like that. So we've been excited with the team's preparation, the very rapid and efficient way that they've been able to work with the FDA. and we're very, very excited about the progress that we've made.

Again, if you have a question, please press star then one. The next question comes from Andy Chen with Wolf Research. Please go ahead.

Thank you so much for taking my question. This is Jason taking it for Andy. I just wanted to ask really quickly about the HLA genotyping, if this is specific for ATTRCM, or do we see this in other indications, like maybe in PN maybe? And do we see any sort of genotyping for maybe some of your other trials coming up? Thank you.

Thank you. currently doing genotyping on a standard basis for any program that we begin. We don't think that that would be necessary, and it would be hard to know what to look for, as we believe that what we're finding here is a very, very specific finding.

And could you repeat your first question?

Maybe, Ed, if you heard it.

I didn't hear it.

Your line is open now, Andy.

Thank you. I just wanted to ask if this genotyping was unique for ATTR-CM, and maybe is this usable in all-linear LFP? Yeah, thank you.

Yeah, no, the genotyping is done across the entire program, irrespective of the indication. and we're treating it as a relevant finding for both polyneuropathy and for cardiomyopathy and are applying the same rules and providing the same information for both studies.

This concludes our question and answer session. I would like to turn the conference back over to Jason Ferdet for any closing remarks.

Thanks, operator, and thanks, everyone, for joining us. We hope you have a great end to the summer, and we'll look forward to seeing many of you at the upcoming conferences in September. That concludes the call.

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.