Scholar Rock Holding Corporation (SRRK) Earnings Call Transcript & Summary

Welcome, everyone, to the 40th Annual JPMorgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JPMorgan. I'm joined by [indiscernible], Priyanka Grover and Caleb Smith from the team. Our first presenting company kicking off the day is Scholar Rock and presenting on behalf of the company, we have CEO, Nagesh Mahanthappa. I want to remind attendees that there is an ask to question feature in the portal. And if you put a question in there, I am happy to ask the question on your behalf. With that, Nagesh, take it away.

Thanks very much, Anupam. Let me get my slides up here. Hopefully you all can see that. Good morning. And again, Anupam can thank you to JPMorgan. Thank you for the opportunity for providing an update this morning on all of the exciting activities at Scholar Rock. Of course, first, the obligatory disclaimer. I will be making forward-looking statements. Full risks are detailed in our SEC filings. And with that, let me first just give you a reminder or introduction to who and what Scholar Rock is. Scholar Rock is a Cambridge, Massachusetts-based biotechnology company focused exclusively on the discovery and development a fully human monoclonal antibody therapeutics. What distinguishes Scholar Rock is we marry cutting-edge recombinant antibody discovery technology with deep structural insights into highly validated biological targets. Targets of interest to us are targets where there's rich biology associated with disease mechanisms, but where there has historically been challenges with actually being able to drive these targets. Our two most advanced programs are focused on members of the TGFß superfamily, our utmost advanced program targeting myostatin. Our next program in line in the clinic targeting TGFß1. What distinguishes our approach in this particular case, while in both of these cases, in fact, is rather than targeting the mature form of the growth factor, we actually target the precursor reforms as shown on the left-hand side of the slide, which effectively turns off the tap, prevents the activation of the growth factor and its availability in the first place, giving us much more potent inhibition of these growth factors. But furthermore, we overcome a traditional challenge in the industry, which is selectivity against these growth factors because of the structural similarity within the active forms. In the precursors, there are structurally differentiated features that we target, which allow us to achieve exquisite selectivity. So looking at the pipeline, apitegromab, this is the monoclinic antibody that targets myostatin selectively prevents activation of its precursor. We completed the main portion of the TOPAZ Phase II study last year, give you a high-level overview of that, very excited to say that we are now in the pivotal Phase III trial. We'll tell you a little bit more about how TOPAZ informs the design of the SAPPHIRE Phase III trial and some further details on that. We'll then turn our attention to SRK-181. This is our antibody, which targets the activation of the precursor of TGFß1, is exclusively selected for ß1 with no [ KRAS ] activity to ß2 or ß3, really a highly differentiated pharmacologic profile, which we are deploying in the context of cancer immunotherapy. I'll tell you a little bit more momentarily about the status of that trial and why it is we believe that targeting TGFß1 in combination of checkpoint inhibitors can actually overcome resistance to check plan inhibitors as manifest in 70%, 80% of patients who received immunotherapy. And finally, I'll wrap up some exciting developments in our preclinical discovery pipeline. So first, turning to apitegromab. Apitegromab is being developed in the treatment of spinal muscular atrophy or SMA. As many of you will know, over the last few years, Three drugs have actually been approved for the treatment of SMA, working across multiple modalities, small molecules, antisense gene therapy, all bringing significant benefit to patients. All of these drugs, however, though they work through different modalities have a common target, which is to effectively up-regulate a protein called SMN, which promotes motor neuron survival, thereby giving benefit to patients. However, there is still significant unmet need for these patients. While these patients are effectively stabilized by these therapies and show some recovery of function, there is clear unmet need and actually improving further motor function and giving these patients overall greater function in their activities of daily living. Now spinal muscular atrophy actually manifests as kind of a spectrum of severity, type 1 being most severe. Type 3, still being manifesting a significant deficit, but not as severe as type 1 or type 2. In our TOPAZ study, which was a 12-month study, we focused on Type 2 and Type 3 patients, which account for roughly 2/3 of the overall patient population and saw what we believe to be truly transformative benefits. Now the manner in which SMA patients are evaluated in clinical trials is to evaluate a variety of different motor tasks and in particular, we make use of a well-validated tool that was used in the development of drugs such as Spinraza called the Hammersmith motor functional scale. This is a 66-point scale, which assesses 22 different activities. And even increases of just a few points are considered very significant for patients. In the TOPAZ trial, what we saw was, again, truly transformative potential in patients with type 2, type 3 SMA. The majority of nonambulatory patients actually showed significant increases over baseline in the Hammersmith scales. And this is what's shown in this waterfall plot here. This is the totality of nonambulatory patients. The upward increase in score shows you the benefit. Some patients seeing increases as much as 20 points and that the vast majority of the patients actually saw a benefit. In fact, when we looked at 12 months, we saw that almost 90% of patients who initiated treatment with nusinersen, background SMN therapy before the age of 5, showed at least a 1 point increase, 63% showed a greater than 3 point increase. And even when we look at older patients, children who started on nusinersen age greater than 5, even up to 1/3 of them saw increases of greater than 3 points. These are really what we view as spectacular results. Now how -- what were the key lessons learned from the TOPAZ study? As I said, the largest Hammersmith score gains were observed in the nonambulatory type 2 and 3 SMA Cohorts. When we did an exploratory post-hoc analysis of these data, we found that where there was the greatest potential for positive effects was in the age group of ages 2 through 12. The robustness of the results were clearly evident after 12 months of treatment. And we didn't see a dose response with a greater effect of 20 milligrams per kilogram versus 2 milligrams per kilogram. These in turn have now influenced the design of the SAPPHIRE study. In the SAPPHIRE study, we are focused on the nonambulatory type 2,3 patients with a focus on the Hammersmith score as our primary efficacy end point. This SAPPHIRE study is focused on ages 2 through 12, 12-month duration with a primary focus on the 20-milligram per kilogram dose. Now that said, let's just go into a little bit more detail about the design of the SAPPHIRE study. As I said, main population ages 2 through 12. There will be three cohorts of 52 patients each. This is a placebo-controlled trial. We'll have the 20-milligram per kilogram dose, dose IV once a week or once every 4 weeks, sorry, on top of SMN up-regulator. We'll have a 10-milligram per kilogram group as well as a placebo group. So again, this randomized, double-blind, placebo-controlled trial. I do want to note that we are going to be enrolling patients who are on nusinersen as well as patients on risdiplam. We're often asked about the enrollment of patients who are making use of gene therapy. I'll just -- foots on the fact that the gene therapies are not yet approved for patients over the age of 2, and hence, our focus on patients who are currently on nusinersen or risdiplam. And finally, on the study, I'd like to say that we are not solely focused on the type 2, type 3 nonambulatory patients. It is -- that is the focus of the SAPPHIRE study. It is ultimately our objective to actually extend the exploration of the treatment of patients with SMA across the full spectrum of disease, including type 1 SMA as well as ambulatory patients. And please stay tuned in the future to hear more about our ambitions for extending the full use of apitegromab in the treatment of patients with SMA and ultimately potentially into other neuromuscular indications as well. So now let me turn your attention to SRK-181, our fully human monoclonal antibody that targets the activation of TGFß1. Now in the field of cancer immunotherapy, as you're all very well aware, there's truly been a revolution with the checkpoint inhibitors. But I think not broadly appreciated still is the fact that of patients treated with checkpoint inhibitors. On the order of 80%, depending on the tumor type, do not actually show benefit. Now what underlies this, based on a wide variety of studies from groups in academia and the industry, highly regarded groups, is that overexpression of TGFß in the tumor microenvironment appears to be a primary driver of resistance to checkpoint inhibition, causing -- this elevation of TGFß causing what is called an immune-excluded phenotype, where lymphocytes are trying to enter the tumor, but seem to gather around the outside we can't get in. What we've come to understand and it's not just any TGFß that is up-regulated in the tumor microenvironment. It is, in fact, TGFß1. SRK-181 is exclusively inhibitor of TGFß1. It avoids hitting ß2 and ß3, which we believe is associated historically with toxicities in that arose from attempts to target the signaling pathway. I'll show you some data to support that for you in a minute, thereby having the selectivity gives us an increased therapeutic window and using as a combination with a variety of checkpoint inhibitors. It has the potential to give us true therapeutic flexibility. Looking at this at a slightly different way to reiterate these points, we believe that the selectivity gives us the potential for improved safety, wider therapeutic window, the ability to combine with any anti-PD-1 or anti-PD-L1 antibody, where we can optimize the dose of both components. And one last point I'll make about the advantage of having two distinct agents used in combination as opposed to a bispecific, is that we believe, based on our preclinical work, looking at the tumor microenvironment, histopathologically, that the spatial distribution of the checkpoint -- the components of the checkpoint signaling pathway versus TGFß signaling are spatially distinct. And so one doesn't actually want to tether the two modes, keeping them separate and optimizing the dose of each individually, we believe is the path towards optimal therapy. Now showing -- just sharing with you some preclinical data. We worked very hard to develop Mouse models that would truly emulate the human situation. So we were able to identify a limited number of mouse tumors, which really behave like human tumors in as much as they show elevated TGFß expression as well as show the immune-excluded phenotype. One example shown here on the top half of this slide, we're looking at data from a Mouse model making use about melanoma. On the left-hand side, you're seeing monotherapy with either the mouse equivalent in SRK-181 or an anti-PD-1 antibody, making a long story short as you look at these growth curves of individual tumors and individual mice, there is not much of an impact of monotherapy. However, if you look at the right-hand side of the slide, you can see the effects of combination therapy are dramatic. Not only are we actually seeing slowing of tumor growth, we are seeing regressions of tumors in the majority of the animals. This correlates with the survival benefit as one might hope in the lower left-hand side of the slide and looking at a different tumor model where we did more expensive histopathologic analysis. This is a bladder tumor model. We find that the combination therapy allows a massive influx in proliferation of killer T cells, which gives us a mechanistic account for why it is we're actually seeing tumor regressions and increase survival benefit. So this gets at overcoming inhibition. Let's speak momentarily about why TGFß1 selectivity is so important. What has been observed historically is traditional inhibitors of the TGFß signaling pathway do not have [ solitivity ] for ß1 per se. They also inhibit the signaling of ß2 and ß3 and associated with that nonselective inhibition of all three growth factors is significant cardiac toxicity, specifically valvulopathy. We've done head-to-head testing of small molecule versus a pan TGFß antibody versus SRK-181 in both rats and nonhuman primates. And what we find is that we can go to just -- I shall say, frankly, whopping high doses as high as 200 to 300 milligrams per kilogram once a week in rats and nonhuman primates, respectively. And at such high doses, we actually see a very clean preclinical profile, not only a lack of cardiotoxicity, but a lack of toxicity in most every organ system and analyzed. So this really speaks to the fact that we think that through the selectivity for ß1, we have the potential for a very broad therapeutic index -- very broad therapeutic window and the ability to maximally hit this pathway hard to overcome resistance to checkpoint inhibition. So we are in, what I'll characterize as the middle of the DRAGON Phase I proof-of-concept study, divide it into two parts. Part A, essentially being the sort of the dose-finding phase to look for safety, PK and to select a dose to move into part B, where we are now -- which we are now in and where we are seeking to look for clear signs of clinical efficacy in specific tumor Cohorts. You can see that Part A itself was divided into two subparts. One was all-comers monotherapy dose escalation, A2 was the combination. Now we are very pleased with what we've learned in Part A so far. We saw a good safety profile, good PK. And interestingly, while we were not expecting to see signs of efficacy per se based on the preclinical work, we did make some interesting observations. In Part A1, for example, we saw 8 patients with the best response of stable disease, three ovarian cancer patients with a response of stable disease and regressions in two of those, quite tantalizing biology, in which we are currently exploring the relationship of TGFß signaling to ovarian cancer. In Part A2, the combinations, again, four patients with the best response. And interestingly, we saw a clear effect in patients with -- one patient with renal cell carcinoma. This has actually influenced how we think about Part B, as you'll see that we've actually added now a clear cell renal cell carcinoma cohort. Now just wrapping up on Part B. We did select a dose. As you can see -- sorry, I have to make an adjustment on my screen. We did pick a dose of 1,500 milligrams once every 3 weeks. Part B encompasses multiple proof-of-concept cohorts enrolling up to 40 patients each. These are patients who manifest primary resistance to checkpoint inhibitor therapy, that is to say they did not respond in the first place. It's not acquired resistance. By selecting these tumors, we've enriched for solid tumor types where we believe there's a higher potential to actually see efficacy signals based on the preclinical biology inside clinical understanding of these tumors. Now I will say that in the times of COVID, it is often challenging to be able to access pre- and post-treatment biopsy samples. And so we've made a significant investment in developing a biomarker strategy such that in particular, we can look at peripheral signs of target engagement and activity of SRK-181. And just to give you a sense of the types of biomarkers we're looking at, I'll focus on one in particular. This is looking at the levels of myeloid-derived suppressor cells or MDSCs. MDSCs are an immune cell type with an immunosuppressive function within the tumor microenvironment that appears to be very important to what may be driving resistance in the tumor microenvironment. Now what we've seen preclinically is that with treatment of the combination of SRK-181 in anti-PD-1, we see a very significant reduction in MDSC levels in the tumor microenvironment. Interestingly, as you can see here on the right-hand side of the slide, not only do we see that reduction in MDSCs in the tumor microenvironment, we see a reduction in MDSCs in the peripheral circulation. This is very exciting because while looking at peripheral MDSCs may not give you a direct readout on impact of the tumor. It's an example of how we can look at a peripheral compartment and more readily accessible patient samples to start looking for signs of activity of SRK-181. And this is just one example of the types of biomarkers we're developing and that we expect to start reporting out on over the course of 2022. So with that, let me just wrap up and say a few words about kind of new horizons and TGFß selectivity as we continue to advance the preclinical pipeline. Now I've made a very significant point of the fact that using our structural biology insights at Scholar Rock, we've been able to overcome the selectivity challenges associated with distinguishing between TGFß1, 2 and 3, and have exquisite selectivity for ß1. But 1 of our endeavor since the beginning of the founding of Scholar Rock was to examine whether we could even get a heightened level of selectivity. Because what we know is that precursor TGFß1 is shown in the cartoons on the right-hand side of the slide is associated with different presenting molecules in different tissue microenvironments. And so in connected tissue or in fibrotic tissue, Latent TGFß1 is actually associated with extracellular matrix protein known as the LTBPs. On immune cells, such as lymphocytes for macrophages it turns out that the pro forma TGFß is associated with a very specific transmembrane cell surface proteins such as GARP and LRRC33. We asked the question, is it possible with Scholar Rock's antibody discovery technology define antibodies that could actually distinguish not only ß1 from ß2 and ß3, but they don't want when it's in the fibrotic tissue versus ß1 when it's on the surface of immune cells. And the short answer is, yes. Yes, we can. And so I'm very excited to share with you some preliminary data. Again, we'll be sharing more with you over the course of 2022. And that when we have found antibodies selected for TGFß1 when it's presented on LTBP in connected tissue, those antibodies actually show exquisite antifibrotic activity in multiple animal models, and show no impact on binding to immune cells. So both on Rat adenine-deficient diet model of kidney fibrosis as well as a Mouse genetic model so-called Alport’s disease modeling, which sees might have a defect in collagen. We see clear antifibrotic effects. An example of those data shown on the right-hand side of this slide, where treatment with an antibody with this LTBP connect tissue selectivity for ß1 show dramatic drops in the phosphorylation of SMAD2 in the nuclei of Alport mouse kidney cells, being a signifier of suppressed TGFß signal. So very exciting results, really speaks to the strength of the Scholar Rock platform and our discovery technology. So my last slide, just to wrap up, to reiterate where we are today, firing on all cylinders at the SAPPHIRE Phase III trial, pivotal trial in spinal muscular atrophy, apitegromab that is ongoing. We are now in Part B of the DRAGON immuno-oncology study, the Phase I proof-of-concept with SRK-181. And we're continuing to build a robust platform of, I'll call it, [ C corn ] for the next INDs. So very excited about what we've accomplished so far at Scholar Rock. And I think 2022 will be a very exciting year for the company. So with that, I will turn it back to Anupam.

Thanks, Nagesh. If you want to introduce the broader team on the line, we can get started with the Q&A.

Yes. That's great. Let me stop the screen share here. And joining me today from Scholar Rock are Yung Chyung, our Chief Medical Officer; and Ted Myles, our Chief Financial Officer.

[Operator Instructions] So Nagesh, you talked about SAPPHIRE and start-up activities have commenced. I think that was announced in late November. Where are you in the start-up activities? What are the -- have you dosed your first patient? How are you thinking about enrollment curve and time lines to data?

Yes. So we haven't gone into great detail publicly on exact status. The sites are being activated. And we're very excited about this trial. We have -- I'll turn it to Yung to speak to some more specifics about kind of trial logistics and what -- and how to think about the pace of enrollment. But I can say we're very excited. The site investigators highly engaged and the patient community is very excited as well. Yung would you like to speak to, what kind of logistics as well as how to think about enrollment?

Yes. Yes. So we're very encouraged by the high level of enthusiasm and engagement, our investigators, trial sites, patient community that we've been seeing to date, trial start-up activities are well underway. Now it's a bit early to try to predict any specific time lines. And this information is not intended as predictor, but rather just as a background point of reference. But the TOPAZ trial enrolled 58 patients across 16 sites in approximately 8 months. Now SAPPHIRE is planned to enroll 156 patients for the main efficacy population across 55 trial sites. And we do have an opportunity for an interim analysis when at least 50% of these participants have completed 12 months of treatment. It really helps that we actually can build off the exciting TOPAZ results showing the therapeutic potential apitegromab. And we believe we have momentum in moving forward with the execution of trials, the SAPPHIRE trial, and we really look forward to working closely with our trial sites, the investigators, the SMA community and progressing the trial as fast as possible.

And what are the levers to thinking about taking that optional interim analysis?

Yes. So we have an opportunity for the interim analysis when at least [ 15% ] of the patients have completed 12 months of treatment. And so the idea of taking a step back is we -- as we thought about the study and powering and sample sizes, we wanted to build upon the TOPAZ insights to really obviously aim to maximize probability and potential for success. Now with that said, we do acknowledge that perhaps we don't need such a large sample size to demonstrate the efficacy of apitegromab. And obviously, there is a high urgency in getting this medicine to patients if our hypothesis is true. And so along those lines, we built in an interim analysis that can take place an opportunity for this interim analysis before we complete the full population to get to 12 months. And so that's why we built it in when at least 50% get there. And so then there's an opportunity to take a look.

And then on the Phase II TOPAZ results, what are the time lines for thinking about [ OLE ] results? When should we be thinking about that?

So the TOPAZ extension study continues to be very important to us in further characterizing the long-term outcomes of patients treated with apitegromab. It's going to continue to provide important efficacy and safety data. And we're very pleased that 55 out of the 57 patients who completed the 12 months of TOPAZ are still in the trial. And they continue to receive treatment and continue to be followed. And so a lot of additional long-term data is going to be collected and analyzed. And our intention is to present further data from the TOPAZ extension such as the 24-month results as well as the digital analysis at upcoming medical conferences, including the Cure SMA conference in second quarter. So stay tuned, a lot coming.

Okay. You've previously also talked about Becker muscular dystrophy, BMD, as an opportunity as a next indication. And I think you've talked about starting a BMD study in 2022. What are the gating factors to that? Is that still the plan? And when can we understand the broader next steps beyond SMA for the drug?

Yes. Again, maybe I'll make an initial comment and turn it back to Yung again. I think our view right now is now that we've described SAPPHIRE, you understand what its focus is. I think our nearer-term goals beyond SAPPHIRE are really to expand the utilization of apitegromab across the broadest possible swath of patients with SMA. Hopefully, all patients with SMA, we believe, in our thinking, could benefit from a apitegromab. So our number one objective is really to maximize that first. And that's where our primary focus is. Above and beyond that, I think that there's the potential across a variety of neuromuscular indications. And I think where we have the potential for further exploration, will be very much in a manner that's similar to SMA in the sense of where can we layer on to an existing therapy to actually improve motor function, but Yung?

Yes. I mean just again, like just to add to what [ Nage ] said, we are -- we think there's broad potential within SMA as well as on neuromuscular indications. So obviously, estimating is very important to us, and so we're going to continue to expand, explore the potential type 1 SMA such as add-on to -- including add-on to background gene therapy, ambulatory SMA, older age ranges, et cetera, very important to us. Now with that said, we think that there is an important potential role to play in other neuromuscular indications. And we're going to apply a lot of the translational insights in thinking about identifying those and pursuing those indications such as conditions for twitch fast twitch fiber deficits play an important role. And yes, so stay tuned, but a lot going on there on that front as well.

I think what's important Anupam is focus right now as we're standing up a Phase III study, and it's the company's first Phase III study is extremely focused on exquisite execution, and that's really a top, top priority. Not to mention the oncology side, which is also a big lift.

Yes. And maybe we'll switch to the oncology side a little bit here. It sounds like we're going to be getting some updates from Part B DRAGON in 2022. How should we think about disclosure here? Is it going to be one robust disclosure? Or is it going to be sort of multiple disclosures throughout 2022? How do we -- individual cohorts, like how do we think about that?

Yung, do you want to speak to that?

Yes, absolutely. So we're very pleased to be in Part B and pleased with the progress with the trial and level investigator engagement that we've been seeing. And importantly, we're enthusiastic about the dose that we identified building upon the Part A results. So just as quick background context, the key hypothesis for SRK-181 in immuno-oncology is embodied by two key questions: Number one, can TGFß1 activity overcome toxicities? They may limit the ability to dose at the levels need for therapeutic effects. And number two, can TGFß1 blockade overcome the resistance of tumors to anti-PD-1, PD-L1 treatment? And so the DRAGON Part A data provided important progress towards that first part of that therapeutic hypothesis. And as we presented at SITC recently, they were no dose-limiting toxicities that they are today. And we were able to escalate to quite high doses of SRK-181. And so the Part A safety data, together with PK data modeling, enabled us to select a dose that we believe is quite robust for Part B. And so we really are excited to test the second part of therapeutic hypothesis and truly see, can this combination approach overcome checkpoint inhibitor resistance. So Partway B is now underway. And it's common with early oncology development, the enrollment and data readouts will be rolling. So we anticipate [ for any ] updates as the data emerge across the various cohorts this year if -- during this year and beyond. But what we really like about Part B is we carefully [ section ] these tumor types for where we believe there's a greater potential for efficacy, opportunities for early efficacy signals. And the fact that it's essentially 5 parallel proof-of-concept cohorts and studies in one. We really think it provides a robust test of hypothesis, and they are excited to see the data as they emerge.

Okay. You guys provided an update yesterday on the Gilead collaboration, having come to an end that you guys have regained your assets from them. Maybe talk about the dynamics of what happened there? And what you plan on doing with these regained assets now that you have them?

Sure. Yes. The Discovery collaboration was very productive. It was -- I think the team is working together did a fantastic job. One of my concerns during the passage of time during that 3-year research period was Gilead was, of course, undergoing some leadership transitions and I think they have put a significant emphasis in their portfolio strategy in oncology. And I think with the reduced focus on fibrosis, they felt that exercising an option on these assets was not the best thing for these assets because we were very enthusiastic about them. They recognized that they had unique pharmacologic activity. And we're really pleased to have them back in the portfolio. In fact, there was a little bit of a frustration to me that given our obligations of confidentiality during the research period that we couldn't talk about some of these very exciting programs. And so that little taste when we provided of LTBP selective connective tissue selective inhibition of TGFß1, it opens up some really exciting opportunities. Now I don't want to kind of oversell that now we're going to become a fibrosis company per se, but I think our ability to generate more development candidates and, in some cases, bring these at least through a clinical proof-of-concept in well-defined patient populations is a really exciting opportunity. So yes, we were pleased with how the collaboration went. Obviously, it would have been great if Gilead wanted to continue the development of these molecules as part of a fibrosis-focused partnership. But absent that, we're happy to continue advancing these programs, really exciting molecules. Edward, do you want to add anything in relation to the Gilead partnership?

No. I mean as you said, they were strategically focused in a different place 3 years ago. And the collaboration ran its course. Teams worked great together. A lot of good outcome, but not strategically aligned for them, it appears. And so we're very pleased to have the assets back in our portfolio.

And then I guess the final question in here. Nagesh, how do we think about sort of time lines to a full-time CEO coming in? You've been leading the shift gear on an interim basis for some months. How do we think about that? And are you on the table maybe to just stay on?

Well, it is not my intention to be long-term CEO of the company. But that said, let me reiterate that there is an active search. We do have a retained search ongoing. And we're being very disciplined about how we want to identify the right candidate. We want to bring on board somebody with seniority and experience, certainly, somebody who's been in the C-suite, if not CEO before. I think clear experience with the commercialization or at least launch and early aspects of commercialization of new products would be important. But this individual could probably come from a variety of different backgrounds. I think the emphasis for us is that he or she should have a breadth of appreciation for the entire enterprise, everything from what will hopefully be an exciting launch of our first product in SMA, but all the way back to the very exciting things we're doing in the laboratory is we're continue to develop the product engine and identify new drug candidates. So I don't have my eye on the exit. My commitment to the company is to stay here as long as it takes to find the right individual. And so my personal focus is the programs, working with this fabulous team with Ted and Yung and others, and just keep the ship sailing in the right direction across all of these activities.

Well, Nagesh and team, I want to thank you guys so much for a super productive session and kicking off the Tuesday of the conference for us.

Thank you so much again for the opportunity to speak today.

All right. Have a great conference, guys. Thank you.

Thank you. You too.