Lexeo Therapeutics, Inc. (LXEO) Earnings Call Transcript

Thank you. Good morning and welcome to Lexeo Therapeutics webcast presentation. [Operator Instructions] As a reminder, this call is being recorded. I would now like to turn the conference over to Ashley Kaplowitz, head of capital markets for Lexeo Therapeutics.

Please go ahead, ma'am. Thank you. Before we begin, I would like to remind you that this call will contain forward-looking statements regarding Lexeo's future expectations, plans, and prospects, which constitute forward-looking statements for the purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in our filings with the SEC. With that, I would like to turn the call over to our CEO, Nolan Townsend.

Thank you, Ashley, and thank you to everyone joining us today. We are excited about the potential of LX2020 and the opportunity ahead of us in PKP2 ACM. We believe this is an underappreciated area within cardiovascular rare disease. PKP2 ACM is a serious progressive genetic disease with no approved treatment designed to modify its course. The affected population is larger than those associated with many traditional rare disease gene therapy indications. With additional data expected this quarter, today's discussion will provide important context on why we believe this is a compelling opportunity, including the clinical disease burden, the scientific rationale for LX2020, and the framework we will use to evaluate clinical treatment response. Later on, Dr. Gasperetti will provide an important clinical perspective on the assessment of ventricular arrhythmia burden in patients with PKP2 ACM. To begin with the disease and significant unmet need, I'll turn the presentation over to our CMO, Narinder Bhalla.

Thank you, Nolan. PKP2 is a serious, progressive, and potentially fatal genetic heart disease. It represents a larger rare disease with a meaningful global commercial potential, including 60,000 affected in the U.S. Disease has both electrical and structural manifestations, with patients experiencing premature ventricular contractions, non-sustained and sustained ventricular tachycardia, progressive ventricular dysfunction, and in the most serious cases, sudden cardiac death. Presentation often occurs in adolescence or early adulthood, creating a lifetime of uncertainty, monitoring, exercise restriction, and treatment burden. The impact is not limited to measurable cardiac events. Patients frequently live with anxiety about whether a symptom may signal an arrhythmia, a looming ICD shock, or disease progression. That is especially difficult for younger patients who may be asked to substantially limit physical activity. Despite the severity and lifelong nature of PKP2 arrhythmogenic cardiomyopathy, there are currently no approved therapies designed to slow, prevent, or reverse the underlying disease. Current management is individualized and may include exercise restriction, beta blockers, and off-label use of antiarrhythmic drugs, catheter ablation, ICD implantation, and in advanced cases, transplantation. These interventions can be important and sometimes lifesaving, but each has limitations. Arrhythmias frequently recur after ablation, and lifelong risk for ventricular tachycardia remains high. Antiarrhythmic therapies may produce partial reductions in arrhythmic activity, but efficacy may be mixed and chronic use can have negative long-term impact. ICDs can terminate life-threatening rhythms, but they do not prevent the underlying disease from progressing. Many patients continue to progress to advanced heart failure, with some ultimately requiring heart transplantation. Devices also carry procedural and lead-related risks, as well as the ongoing burden associated with the possibility of a painful shock. The unmet need therefore extends beyond symptom control. Patients need a therapy that targets the genetic root cause and has the potential to improve the electrical and mechanical consequences of PKP2 deficiency. LX2020 is an AAV RH10-based gene therapy designed to deliver a full-length functional PKP2 gene to cardiomyocytes. PKP2 is a key component of the desmosome, which helps maintain the connections between heart cells. When PKP2 is deficient, those connections are disrupted, contributing to electrical instability, mechanical dysfunction, and progressive cardiac injury. By restoring PKP2 expression, LX2020 is designed to potentially address the biology underlying both of the electrical and structural manifestations of the disease. PKP2 is not a one-dimensional disease, and no single measure captures its full biological and clinical burden. We think about treatment response across three complementary domains. The first is arrhythmic activity, including PVC burden, NSVT, and sustained ventricular arrhythmias. The second is myocardial structure and function, including strain, contractility, ventricular size, and ejection fraction. Third is the patient and clinical burden, including symptoms, treatment escalation, hospitalization, ablation, ICD shocks, and other consequential patient-related outcomes. These measures may evolve on different timelines with electrical changes potentially emerging before structural remodeling. For today's discussion, I'll focus primarily on the arrhythmic domain. Ventricular rhythmic activity can present in several forms. Premature ventricular contractions, or PVCs, are premature beats arising from the ventricles. They can occur frequently and provide a quantifiable measure of ventricular ectopic activity. NSVT represents a different pattern. Rather than isolated or separated ectopic beats, NSVT, as defined in the cardiovascular clinical guidelines, consists of at least three consecutive ventricular beats at a rate greater than 100 beats per minute, terminating spontaneously in less than 30 seconds. Sustained ventricular tachycardia persists for at least 30 seconds or requires earlier intervention because of clinical instability. Other clinically consequential outcomes include ICD therapy and sudden cardiac death. These events are related, but they're not interchangeable. Not every PVC progresses to NSVT. Each provides different information about ventricular electrical instability. Both PVC burden and NSVT provide relevant information about ventricular electrical substrate in ACM. However, they measure different features. PVCs are prevalent, and PVC burden measures how frequently ventricular ectopic beats are occurring. Because most patients with PKP2 ACM have high PVC burden, it is an important measure and a target to measure potential treatment response. PVCs, however, may be influenced by external factors such as exercise, stress, caffeine intake, and can fluctuate significantly over time. Furthermore, a large change in the PVC burden may not always trigger a meaningful change in treatment. NSVT is made of ventricular beats, which occur consecutively as a burst lasting less than 30 seconds. This reflects greater arrhythmic complexity and has a stronger established relationship with clinically consequential outcomes such as sustained ventricular tachycardia or ICD discharge. For this reason, NSVT is a major factor in ACM risk assessment, whereas PVC burden is a minor factor. Any incidence of NSVT is considered clinically meaningful and increases the risk of future ventricular tachycardia. As we evaluate the therapeutic impact of LX2020 across endpoints, we've developed a framework for how to best interpret PVC burden and NSVT, particularly when the measures do not move in the same direction. This matrix provides a framework for that interpretation. Rather than assigning significance to either measure in isolation, we consider the pattern across both measures, the magnitude and durability of the changes, and the broader patient-level dataset. This consistent framework informs our interpretation of the data presented to date and will guide our assessment as the dataset matures. Importantly, the reason NSVT carries particular weight within this framework is its established relationship with clinically meaningful outcomes. Ultimately, we would hope to see both measures decreasing over time in the majority of the patients, but given the regular fluctuations in PVCs observed in PKP2-ACM and the susceptibility of this measure to external factors like exercise, we might interpret reduced NSVT as a more meaningful reduction in clinically significant arrhythmias despite a lingering PVC burden. The clinical relevance of NSVT is supported by evidence across multiple studies. NSVT is not simply a more complex rhythm observed on monitoring. Its presence is associated with meaningful downstream clinical risk, where patients with NSVT had approximately two and a half times the risk of subsequent sustained or life-threatening ventricular arrhythmic events. NSVT also informs clinical practice. Its detection may prompt additional monitoring and risk assessment and can contribute to decisions involving medication, ablation, surveillance, and primary prevention ICD therapy. PVC burden alone is unlikely to prompt ICD implantation or surgical ablation, for example, but NSVT almost always triggers a clinical intervention. Finally, NSVT can be assessed objectively through ambulatory monitoring using defined beat count, rate, and duration criteria. It provides a clinically grounded and consistently measurable framework for evaluating NSVT in our clinical program. Having established why NSVT is clinically important, I want to explain how we are defining and assessing this measure in the LX2020 clinical program. In our January 2026 data cut, we evaluated and presented NSVT as total ventricular runs, defined as three or more consecutive ventricular beats at any rate. That approach allowed us to capture the full spectrum of consecutive ventricular activity observed on ambulatory monitoring. As we progress discussions with regulators and work towards establishing an endpoint with the highest clinical relevance in ACM for the purposes of a future registrational trial, we have focused on guideline-defined NSVT. At least three consecutive ventricular beats at a rate greater than 100 beats per minute, terminating spontaneously within 30 seconds. This is a definition used in the clinical guidelines, in ACM literature, and in established risk frameworks. As the most common clinically significant manner in which to measure NSVT, it will be the basis of our assessment going forward. The distinction is illustrated by the examples on the slide. The 4-beat run at approximately 85 beats per minute is included in total ventricular runs, and it reflects a clinical abnormality, but it does not meet the rate threshold for guideline-defined NSVT. The 5-beat run at approximately 150 beats per minute is included in both the prior and current measure since it qualifies as guideline-defined NSVT. Importantly, this does not change the underlying ECG recording or the ventricular activity that occurred. It provides a more clinically meaningful way to classify that activity and evaluate change over time. Turning to the patient-level baseline, this slide shows the guideline-defined NSVT data that will anchor our evaluation of LX2020 going forward. The event counts are lower than total ventricular run counts because slower runs that do not meet the greater than 100 beats per minute threshold are not classified as guideline defined NSVT. Every participant, however, had at least one qualifying NSVT event at baseline. That matters because established age is not a factor. ACM risk frameworks recognize a history or presence of NSVT as a clinical risk marker. Any presence of qualifying NSVT is therefore clinically relevant, even before considering the total number of events. Importantly, we do not expect the effect size to be diluted because of the updated baselines. In practice, I looked at PVC burden and NSVT differently. A modest change in the PVC burden may not by itself materially change my assessment of a patient's arrhythmic risk. The detection of NSVT, however, did change that assessment and prompted consideration of closer monitoring, a change in treatment, or depending on the patient's overall risk profile, an ICD implant, or a change in the settings of a previously implanted ICD. At the same time, presence and burden provide different information. One qualifying event established as NSVT occurred, while the number of events provides additional information about the patient's overall arrhythmic burden and risk. For that reason, we will evaluate both the presence of NSVT and changes in the burden over time alongside PVC burden and other outcomes. This provides a clinically grounded and consistent framework for evaluating treatment responses as the LX2020 dataset matures. Now, putting this into context as we think about the upcoming readout, our first consideration will be whether LX2020 produces a meaningful reduction in clinically relevant arrhythmic activity. NSVT will be an important clinical lens with PVC burden, safety, and the broader patient level dataset providing essential context. If the current care results in 20 to 30% relative reduction in the risk of NSVT, a benefit beyond that in the 35 to 40% range with a favorable safety profile should be extremely meaningful for patients and physicians, particularly since currently used treatments such as flecainide and amiodarone may have significant side effects and do not address the progression of heart disease. This benefit can be measured in a number of different ways. For example, it can be looking at a change from baseline, or it can be understanding the number of patients that fall below a particular threshold with a treatment at a given time point. Seeing a sustained or deepening effect is also important, and we want to see an effect size materially better than current care with the guideline-defined NSVT baseline. Because it may take time for the biological effects of gene therapy to translate into clinical benefit, we would want to see the effect maintained and potentially deepened over time. Finally, safety will remain central to the benefit-risk profile of LX2020. The patients we are targeting may be earlier in the disease journey and are considering a one-time genetic therapy. A favorable safety profile together with meaningful and durable arrhythmic improvement would support the potential of LX2020 to change the treatment paradigm. The upcoming readout should offer insight not only into the clinical profile of LX2020, but also provide greater clarity on the path forward for the program. We remain on track to provide a regulatory update concurrently with the readout this quarter. To help put this framework into clinical context, I'm pleased to welcome Alessio Gasperetti, M.D., Ph.D., of Cleveland Clinic. Dr. Gasperetti, thank you for joining us.

Oh, absolutely. Thank you for having me today. So my journey into management of ACM patients has been quite long. I have the privilege of working with those patient population across Europe and the United States over the last decade, give it a take. I started taking care of those patients in Europe and Milan, Italy, one of the largest EP centers. There, under the guidance of Professor Tondo. I did one of my postdocs at the University of Zurich, which has very large registry for patients with arrhythmogenic cardiomyopathy. And then I came to the United States where for seven years, I was in a joint tutelage under Dr. Calkins at the Johns Hopkins University where they have the largest arrhythmogenic cardiomyopathy center in the world. And I was working also with the team in Utrecht. So I really got a good exposure during my training and during my early years to high volume centers taking care of a large array of patients with arrhythmogenic cardiomyopathy, right-sided, left-sided, biventricular. It's been very exciting. Now I'm at the Cleveland Clinic and we're doing good work here too. So it's been a long journey, but I've certainly learned a lot and it has been very, very exciting to see all the new changes and improvements that have entered the field.

Great. Hey, thanks for that. And then, you know, as you kind of think about ACM and arrhythmogenic cardiomyopathy, particularly PKP2 associated, you know, can you give us a little bit of a sense as, you know, from your perspective, how do you see, you know, the unmet need? And what are you thinking about when you see a patient who has PKP2 associated ACM? How are you trying to understand where they are in their disease journey, and how are you assessing them initially?

Oh, this is a fantastic question. So anytime you see a patient with arrhythmogenic cardiomyopathy, I think you've got two questions to answer in front of you. Where is that patient in their journey right now? And where are they going to be in five years? And the reason for that is that this is a progressive disease. So my role as a clinician is to make sure that this patient is safe today, right now, but that I'm also trying to steer the disease progression away from, you know, bad outcomes down the line. And this is sort of a story of two clinical outcomes in this patient. This patient suffers from pretty gnarly arrhythmias. We know that sudden cardiac death from ventricular arrhythmias is really the main cause of death in the early stages of this disease. But down the line, this is also a progressive disease that can cause pretty advanced heart failure. And if untreated, this patient can progress to Stage D heart failure and require heart transplantation. So it's always good, the first thing is to get a sense where they are right now. Are they in a more arrhythmogenic phase of the disease, or are we already seeing signs and symptoms of heart failure? And very often the first question that we need to answer is, does my patient need a defibrillator right now? So risk stratification and specifically arrhythmia risk stratification plays a crucial role in our first interaction with the patient. So it's a lot of data gathering, getting a sense of where they are mentally, clinically and physically, and trying to see what I can offer them at the get-go.

Thanks. And so, you know, you talked about the risk assessment, you talked about the arrhythmia risk and trying to understand that risk a little bit better within the assessments that you do initially. Can you think a little bit, can you tell us a little bit about how you look at the various arrhythmias such as PVCs, NSVT, and the risk of ventricular tachycardia? And a bit about, you know, how do you interpret these different measures more clinically regarding clinical importance and overall burden, et cetera.

Absolutely. So, we always try to use a multi-modality assessment of those patients. So, whenever we get a Zio patch or a Holter, we always pay a lot of attention to the PVC burden. Most centers tend to use an average burden over 24 hours, a lot of attention of non-sustained ventricular tachycardia. Historically, the field has used non-sustained ventricular tachycardia as a binary outcome. So a patient either has it or does not have it at a specific time and place. But over the last few years, there has been a lot of interest and try to see what is the value of the burden of non-sustained ventricular tachycardia as well. And those two metrics give us very different signals and very different information about the patient. Most of the current risk stratification strategies, both at a European and an American level, combine those two parameters, so they're both important. But if we look at, for example, the ARVC risk calculator implements both of those metrics, it is very clear that the relative weight of those two is somewhat different. If we look at the PVC burden, which is generally measured as a logarithmic assessment, with risk and the NSVT, the presence of non-sustained ventricular tachycardia has somewhat two-fold the magnitude of prognostic value that the PVC burden has. So really, both are important metrics, but I think that whenever it comes down to what a more predominant marker of arrhythmia risk, probably the presence of non-sustained ventricular tachycardia seems to be more important.

Thanks. Yeah, I think that's an interesting point about just the different weight that you would look at from the standpoint of NSVT versus PVC burden. One of the other things that I wanted to ask you a little bit about is, albeit it may seem simple and straightforward, but, you know, defining NSVT. How do you as clinicians and then also look at what the guidelines say, how are you defining NSVT when you're reading a Holter monitor or looking at a Zio patch, et cetera?

Well, that's such a good question because we all need to speak the same language in order to understand our data. I think that the ARVC community and the arrhythmogenic cardiomyopathy community as a whole, starting at least in 2018, 2019, has somewhat come to an agreement that our definition of non-sustained ventricular tachycardia, and this is what has been reported, across probably the last decade of scientific studies has been three or more ventricular beats in a row, total episodes lasting less than 30 seconds with a heart rate of around 100 beats per minute or more. So it's a fairly standardized definition with pros and cons, but it has served us well and has really helped us risk stratifying those patients.

Thanks, and I think that's important only because, and you just said that, that also when you look at the literature and how the published literature is defining this is with that format. So I think it's important to make sure that we're all singing from the same hymn sheet, so I appreciate that. Thank you. Of course. So just keeping that lens a little bit more, how do you think about, you know, how do you manage these differentially, let's say, in the terms of disease management when you see a patient who has both the PVC burden and also having episodes of NSVT? And as you're talking about that a little bit, can you also talk a little bit about, you know, you talked about this feeling of NSVT, but talking a little bit about, you know, what is the low burden of NSVT? What is the meaningfulness of that versus a higher burden? Because, you know, there's this sense that maybe a low burden of NSVT is not as clinically meaningful. So just trying to get a sense of how you see that and how do you assess and manage these arrhythmias differentially.

Absolutely. It's a wonderful question. And I'll probably start from the back end of it, just because around 50% of the people with arrhythmogenic cardiomyopathy will come through a clinic or, you know, will get admitted with a combination of PVC and NSVT. In those two, if those two are present, we manage both and we use both as a good marker of risk stratification. But there is probably around a quarter of patients with arrhythmogenic cardiomyopathy, they will be evaluated, will be found having a very low PVC burden, and yet, they do have non-sustained ventricular tachycardia. And just because the burden of non-sustained ventricular tachycardia is low, the number is low, like one or two episodes on a Holter, it doesn't mean that we can ignore that data point. If anything, that data point is actually very important because that's the main marker of arrhythmic disease of a specific patient. Just to give an idea, most of the current risk stratification strategies use NSVT, as I mentioned, as a binary outcome, so the presence of one or two runs of NSVTs on a Holter will put patients into a completely different bin of arrhythmic risk to the point that the presence of non-sustained ventricular tachycardia can easily trigger at least the consideration for an ICD implantation in a patient in an independent way from the patient, the PVC burden. So just because the number is low doesn't mean that the effect size is low. Clearly, a much higher number means a much higher risk, but just a low number doesn't automatically correlate with an absolute low risk of arrhythmia. Now, when we try to get a sense of what's a meaningful change and how do we like to see those numbers change over time? Well, you know, in an ideal world, if a patient has non-sustained ventricular tachycardia, a couple of runs, a few runs over a Holter or a Zio patch recording, ideally, I would like those to go away. I think that if we have a normalization of non-sustained VT burden to the point that they completely disappear. I think that we are really stabilizing the risk of this patient. I will also acknowledge that sometimes patients come in with a much higher non-sustained VTAC burden and it may be impossible to reach zero over a small period of time over the single intervention. So right now we do have a few data out there from a few of the interventions that have been attempted in this patient population, probably thinking about data from Flecainide showing very good clinical response in this patient. We have seen around a 30% drop in NSVT burden, specifically around 25 to 30% of patients that had non-sustained ventricular tachycardia before the pharmacological intervention. Really become non-sustained ventricular tachycardia free during follow-up. I think this is a reasonable drop to aim for in a therapeutic intervention, acknowledging that not all my patients will have non-sustained V-tach, but those that have, if I get around a third of them, NSVT free, 40% of them NSVT free, a good 30 percent drop in their burden, those that are not NSVT-free, I think that's a reasonable clinical outcome to aim for.

So as you think about that, you know, when you think of those numbers that you kind of talked about from the standpoint of reduction and what could be clinically meaningful from a reduction perspective, how do you, when you then kind of bring gene therapy into the mix and LX2020, which is our program, how do you start to think about what would be a good bar for gene therapy to strike that would be clinically meaningful, not just for you as a clinician, but also for your patients that would make sense for you to say, hey, you know what, this is a treatment that's met the bar that would be set?

Oh, that is a phenomenal question. And I think it truly goes down to how therapeutics are affecting the natural course of disease in arrhythmogenic cardiomyopathy. And the real answer is that none of the medication that we're currently using, none of the intervention that we're currently applying to those patients is really changing the natural history of disease. The gene therapy, both your program for sure, has the potential of changing the long-term trajectory of disease. So, you know, whenever I prescribe medication and I'm achieving a reduction in PVC burden and a reduction in non-sustained VTAC burden, I'm somewhat stabilizing my patient, but I'm not doing anything for their overall risk of structural disease progression over the decade. And I'm not significantly impacting the risk of heart failure down the line. Probably exercise reduction is the only thing that plays a significant role in that alley. But certainly, I don't think we have convincing data from any of the medications. Therefore, I think, you know, gene therapy strategy, has the unique opportunity or the unique feature of being potentially able to change the whole natural history of disease. And that's why I think they're so appealing to clinicians, but also to patients, because the idea is that we are changing their structural components and potentially we're altering the progression of disease. So probably if we are achieving a similar bar of arrhythmia reduction that we have achieved with medications, we are in a very good spot because, you know, if we are tying in terms of efficacy with flecainide or with beta blockers or with exacerbation reduction, and on top of that, we also have the potential for reducing heart failure down the line, I think that's a very reasonable clinical expectation from this sort of novel therapeutics, fully acknowledging that in most trials we won't be able, even probably in a Phase 3 trial, we will not be able to see a meaningful heart failure or heart transplant reduction down the line just because this is a progressive disease that progresses over a timeline that is measured in multiple years. We're looking at maybe five to 10 years to see really the heart failure kicking in from the onset of the diagnosis. But I think the potential of preventing that is there, and that will be incredibly valuable.

For patients and clinicians alike. Thanks. So as we kind of come to a close on this, any last thoughts that you want to leave the audience with when it comes to PKP2-related arrhythmogenic cardiomyopathy management, NSVT, how do you think about gene therapy, et cetera? I know we've talked a lot about it, but anything that you want to add to the discussion we've just had?

Yeah, I think, you know, gene therapy in this patient population is a very exciting tool that is coming into our tool set. I don't think that every patient will automatically qualify for this kind of intervention, but I think that there is certainly a significant niche, and not even niche at all, but a significant portion of patients that down the line could really benefit from this. The arrhythmic components that we have discussed, I think that the most important points that I would really like to reiterate because we discuss among colleagues about this all the time. Now, sustained ventricular tachycardia are important. And over the years, we kind of forgot about the concept of burden. Arrhythmogenic cardiomyopathy has used this binary outcome for probably too long. I think our colleagues in hypertrophic cardiomyopathy have implemented burden analysis much earlier than we did. I think really taking into consideration all the different points in the multidisciplinary and multi-system assessment of this patient is important. And also reminding that we are managing the arrhythmic risk today with the hope of managing heart failure down the line with a single therapeutic is a really important topic that I think should always be mentioned when we talk about the pros and cons of these therapeutics. Cool.

Great. Dr. Gasperetti, thank you for sharing your perspective and for helping us take these measures in the context of clinical practice. That concludes our discussion. I'll now turn the call back to Nolan for closing remarks. Nolan?

Thank you, Nani, and thank you again, Dr. Gasperetti, for joining us today. I want to close by connecting the clinical discussion back to the broader opportunity for LX2020. Based on the addressable population and the potential value of a one-time disease-modifying therapy, we believe LX2020 represents a multi-billion dollar market opportunity. The program also benefits from practical development and commercial advantages. Patients are concentrated across a relatively small number of leading, specialized heart failure treatment centers worldwide, creating a meaningful global opportunity, providing access to a substantial, identifiable patient population that can support rapid clinical trial recruitment and future commercial uptake. Our manufacturing platform at Lexeo is designed to support scalable and cost-efficient supply for a population that is one of the most prevalent disease area opportunities in gene therapy. Ultimately, the commercial opportunity depends on delivering a therapy that meaningfully changes the course of disease. That is why the clinical framework we have discussed today and the additional data expected this quarter are so important. We remain excited about the potential of LX2020 and look forward to sharing the additional clinical data. Thank you for joining us. I'll now turn the call back to the operator for questions.

Thank you. [Operator Instructions] Our first question is going to come from the line of Roanna Ruiz, Ph.D., with Leerink Partners. Your line is open. Please go ahead.

Hey, everyone. A couple from me. I appreciate your comments about NSVT being the more clinically meaningful endpoint. And as a follow-up, could you just walk us through what supports your confidence in being able to enroll patients with sufficient NSVT burden? Could that be a hurdle for a pivotal? Or if not, could you walk us through why?

Thanks, Roanna, for the question. I would say, first off, you can see the patients in our study, the vast majority had an NSVT burden at baseline. So even in this study of 10 patients, we were able to find a meaningful number of patients with an NSVT burden at baseline.

I don't know, Nani, if there's anything else you'd want to add to that. No, and I think as Dr. Gasperetti was talking, recognize that almost 85%, 90% of patients, if you total up those who have PVCs and NSVT, and then those who have low burden of PVCs, but also have, you know, pretty much primarily only NSVT, I think you're looking at a very large majority of the population that has enough burden of NSVT to enroll into a.