Voyager Therapeutics Inc (VYGR) 2022 Q3 法說會逐字稿

Good morning, and welcome to Voyager Therapeutics Third Quarter 2022 Conference Call. (Operator Instructions) Please be advised that the call is being recorded at the company's request. A replay of today's call will be available on the Investors section of the company's website approximately 2 hours after the completion of the call. I would now like to turn the call over to Pete Pfreundschuh, Chief Financial Officer.

Thank you, and good morning. We issued our third quarter financial results press release this morning. The press release and 10-Q are available on our website. We plan to be very efficient in today's call. Accordingly, we are going to provide a brief summary of key highlights from the quarter and reserve the majority of time for your Q&A.

In a moment, I will turn over the call to Al. Before I do this, I want to remind everyone that during this call, Voyager representatives may make forward-looking statements regarding future expectations, plans and prospects. All forward-looking statements are inherently uncertain and subject to risks and uncertainties that may cause actual results to differ materially from those indicated by these forward-looking statements. You are encouraged to review and understand a number of the material risks and uncertainties facing the company as described in the company's annual report on Form 10-K filed with the SEC as updated by subsequent SEC filings, including the company's most recent quarterly report on Form 10-Q filed this morning. All SEC filings are available on the company's website.

Now it is my pleasure to turn over the call to Voyager's Chief Executive Officer, Dr. Al Sandrock.

Thank you, Pete, and good morning, everyone. I'd like to start by summarizing Voyager's investment thesis. Voyager is a biotechnology company dedicated to breaking through barriers in gene therapy and neurology. The potential of both disciplines have been constrained by delivery challenges. Gene therapy has been limited by narrow therapeutic windows and associated safety issues. Neurology is limited by the difficulties of getting larger molecules across the blood brain barrier. At Voyager, we are leveraging cutting-edge expertise in capsid discovery and deep neuropharmacology capabilities to address these constraints, which we believe will ultimately create significant value for patients and shareholders.

We have created 3 pillars of value at Voyager. First, our TRACER capsid discovery platform is generating breakthrough capsids to fuel both our own pipeline and that of partners, including Neurocrine, Pfizer and Novartis with significant potential for future partnerships. At the core of TRACER is our proprietary expression-driven in vivo screening system. This has allowed our team to evaluate more than 20 million variants of AAV5 and AAV9 capsids and select only those capsids that display increased transduction in the target organs. We have started by targeting the central nervous system. And in preclinical studies, we have demonstrated more than 100-fold higher transgene expression in the brain compared to conventional AAV9 capsids.

We have also demonstrated blood-brain barrier penetration across multiple species, including mice and nonhuman primates, which increases our confidence that we may be able to translate these properties to humans. At ESGCT last month, we presented data on a novel capsid that demonstrated high levels of CNS gene expression when administered intravenously in the range of 2% to 20% of the doses used by conventional capsids, potentially improving the therapeutic window of gene therapies.

Further, we presented data characterizing a novel cell surface binding receptor for one of our capsids families, and we confirmed the analogous function and expression of this receptor in humans. In the near term, this discovery further increases our confidence that the preclinical results we are seeing may translate into human clinical trials. In the longer term, this receptor could enable reverse engineering to further enhance the capsids generated by our TRACER platform.

In addition, we have begun experiments to explore whether we may be able to leverage this receptor to enable the delivery of therapeutic modalities such as proteins and oligonucleotides across the blood-brain barrier, which if successful, could constitute a new platform for CNS drug development. The novel capsids derived from TRACER have attracted the interest of multiple partners, including Pfizer and Novartis, and additional discussions are ongoing with multiple pharmaceutical companies. Pfizer's decision in September to exercise their capsid option triggered $10 million of revenue and $30 million in deferred revenue in Q3 2022.

Our second pillar of value is our transformative CNS pipeline. I will review our progress advancing the pipeline in just a minute, but I want to call out that each of our 3 lead programs are directed against targets validated by human genetics and human biology. Moreover, they exploit the availability of biomarkers to enable a path to quickly and efficiently achieve proof of biology. As we said in our Q2 call, we expect to identify these candidates later this year and into the first half of next year, laying the foundation for IND filings in 2024 and 2025. We also note we are targeting serious life-threatening diseases that create significant burdens for patients and caregivers, Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis or ALS.

Our third pillar of value is our sound balance sheet, enabled by our track record of generating non-dilutive partnership revenue. As of September 30, 2022, we reported cash, cash equivalents and marketable securities of $132 million. Our balance sheet position along with amounts expected to be received as reimbursement for the development costs under the Neurocrine collaboration, are expected to be sufficient to meet Voyager's planned operating expenses and capital expenditure requirements into 2024. Pfizer's exercise of its licensing agreement triggered a $10 million cash payment in Q4 2022. Additionally, the potential option exercise by Novartis prior to the option expiration date in Q1 2023 would enhance the company's operating runway further. The company has no debt obligations to third parties.

I want to make one more point here, which is that our capsid licenses are structured around this target, not the capsid. Once our partners select their gene of interest, we don't work with anybody else on that gene, but it is entirely possible that multiple partners may select the same capsid, and we may also select that capsid for some of our own internal programs. The benefits of this structure are 2-fold. First, because these deals are not exclusive to the capsid, we have the optionality to continue to pursue partnerships. Second, as some of our partners do choose capsids that we also utilize in our own programs, they may provide initial clinical validation of our capsids.

I want to dig a bit deeper to the pipeline now. Voyager continues to advance our 3 prioritized programs, a humanized anti-tau antibody for Alzheimer's disease, SOD1 gene silencing for ALS, and GBA1 gene replacement for Parkinson's disease. In addition to these 3 programs, I want to remind you that we have a collaboration ongoing with Neurocrine to develop a gene therapy for Friedreich's ataxia, which Neurocrine is currently funding through Phase 1. At that point, Voyager has an option to co-develop and co-commercialize the asset in the U.S. at a 40-60 cost and profit split with 40% coming to Voyager or to grant Neurocrine full global commercial rights in exchange for milestones and royalties.

Our tau antibody program is being developed as an IV delivered passive immunotherapy. Research has shown that tau pathology propagates across certain brain regions in a well-known pattern in Alzheimer's disease. The spread of tau pathology can be monitored with PET imaging, and we plan to use this biomarker to establish early proof biology. Our therapeutic hypothesis is than an antibody targeting tau may block the neuron-to-neuron spread of tau at several plausible extracellular sites. Our antibody is differentiated from other antibodies that have not demonstrated clinical efficacy and that our antibody targets the C terminal rather than the N terminal region, and it has been shown in preclinical models to significantly reduce the spread of pathological tau. We are on track with our work to [immunize] the murine antibodies.

Moving now to GBA1 Parkinson's disease. Up to 10% of Parkinson's disease patients have mutation in GBA1, the most common genetic risk factor, increasing the risk of disease approximately 20-fold. GBA1 encodes the lysosomal enzyme, glucocerebrosidase or GCase, and we believe restoration of GCase in Parkinson's patients with GBA1 mutations will have therapeutic benefit. GCase levels can be measured in CSF as can be substrates of GCase that are abnormally elevated in GBA1 carriers due to the loss of function mutation. These biomarkers provide a potential path to early clinical development derisking. Our approach combines the GBA1 gene replacement with a CNS-tropic, BBB-penetrant, novel TRACER derived capsid. NHP studies to select our lead candidate are underway.

And now SOD1 ALS. ALS is a rapidly progressing neurodegenerative disease that typically leads to death approximately 3 years after diagnosis. We believe that by silencing expression of the SOD1 gene in the CNS, we can provide therapeutic benefit to ALS patients with SOD1 mutations. Proof of concept for this approach has been demonstrated by tofersen, an investigational drug sponsored by Biogen and Ionis, which is currently under review by FDA. SOD1 is measurable in CSF and can serve as a biomarker for early efficient proof of biology in a small clinical study. Serum neurofilament light chain will also be measured to determine whether or not there is a signal of efficacy.

Our approach combines a potent siRNA construct with a CNS-tropic blood-brain barrier penetrant, novel TRACER derived capsid. NHP studies to select our lead candidates are underway. We continue to expect to identify lead development candidates for all 3 programs between Q4 2022 and H1 2023. These lead candidates will then be advanced into IND-enabling studies to support IND filings expected in 2024 and 2025.

I also want to note on this slide that we have several partnerships using novel TRACER generated capsids. As I mentioned above, any progress by our partners may provide even earlier clinical validation.

In summary, we believe Voyager has demonstrated strong validation of our ability to execute during the third quarter and the subsequent period, and the company is gaining momentum as we closed out 2022 and look towards 2023. In addition to advancing our pipeline, we continue to build out our Board of Directors as well as our executive team. We appointed Dr. Kitty Mackey to our Board. We also added Pete Pfreundschuh as CFO; and Trista Morrison as Senior Vice President of Corporate Affairs, and we promoted Dr. Todd Carter, the Chief Scientific Officer.

We also presented encouraging preclinical data at the AAIC and ESGCT conferences. Those posters are on our website if you haven't seen them. And we saw a further validation of our TRACER platform from Pfizer's decision to exercise its option. Looking forward, we continue our work to break through the barriers constraining the fields of gene therapy and neurology. We look forward to identifying lead candidates for our 3 prioritized pipeline programs between the end of this year and the first half of next year, and we will keep you updated as we advance towards INDs. We will continue to share the exciting data we have generated at scientific conferences. We also have the initial Novartis option exercise decision coming up by March of next year.

I want to take a moment to acknowledge everyone on the Voyager team. I've been CEO of this company for about 7 months now, and I am so excited to be working with such incredibly talented scientists and other professionals. With that, we're happy to take any questions you may have. Joining me today for Q&A are Pete Pfreundschuh, our CFO; and Dr. Todd Carter, our Chief Scientific Officer. Operator?

Thank you. At this time, we will conduct a question-and-answer session. (Operator Instructions) Our first question comes from Jack Allen with Baird.

Congratulations to the team on the progress throughout the quarter and Pete and Todd for the new roles as well. I guess my first question was around the selection of development candidates moving forward. I was wondering if you can provide any color as you look to select these development candidates around, how you're thinking about capsid selection? Would it be your goal to have an overlapping capsid strategy? Or would you look to kind of diversify within the capsid library of future capsids that you have for different assets? I'd love to hear your thoughts as it relates to that.

Thanks, Jack. This is Al, and I will start and I'm sure Todd will want to jump in. But look, we have capsid profiles for each of our programs, where the scientists said, these are the characteristics that are ideal for this disease, depends on which cells need to be transduced, what regions in the brain, et cetera, and also the targeting issues. And so we will select the best capsid. Now it may be that there are obviously advantages, if we use the same capsid for multiple diseases, certainly manufacturing for example. But I think our approach is, we want to use the very best capsid for the patients, so that we can treat the patients in the most optimal way. Todd?

I think you've captured it quite well.

Thanks, Todd.

Great. And then if I could just ask one follow-up on the appetite for future partnerships. You made another remark on the call that you have ongoing conversations, and those conversations seem to have been going on for quite a bit. I'd love to hear any thoughts as to how the conversations are going and how investors should think about potential near-term updates as it relates to additional future partnerships?

Yes, Jack. Well, I mean we are having ongoing conversations with multiple parties, and we're open for business. We're open to partners certainly on our capsids because I mean, look, everybody else sees that we're breaking barriers too for gene therapy. And we're also open to partnering on our programs, either programs or capsids we're open to anything really. And I have to say, as for myself, I am enjoying these conversations, many of them with former colleagues.

Our next question comes from Phil Nadeau with Cowen.

A follow-up on the selection of the lead candidates with the GBA1 and SOD1 therapies. Can you talk a bit more about what measures you're able to capture in the nonhuman primates to select between candidates? Is it simply a transduction of certain brain areas and safety? Or are there biomarkers and other measures that will inform your decision?

Todd, do you want to take that?

Sure. So yes, the answer to your question is we're looking at a number of things. So going with the gene therapy, we look at vector distribution, where does the therapy go? We look at the level of expression off of that vector. So we're looking not only at where the vector goes, in the case of GBA, GCase activity, the protein, the enzymatic activity in the case of SOD1-ALS program, the amount of knockdown we achieved in the relevant brain regions. We also look at where we hope to not go. So the off-target tissues that Al mentioned earlier, we look at capsids. So we look at all of those components. In addition, for something like the GBA, we can look in the fluid compartments, such as the cerebrospinal fluid for delivery into that space as a marker and a correlate for how much transduction or delivery we get into the brain. And that's something that we're hoping to use as we move forward into the clinic as well.

And just one follow-up. In your experience, how predictive is the NHP model of what happens in humans, appreciating it's probably the best model that we have, how much uncertainty remains after you see these measures in the NHPs?

Well, so for our novel capsids, they're novel capsids. We have identified a receptor for one capsid family, which we think gives us increased translatability into humans. But until we actually do the human experiment, we won't know for sure. I think that the delivery of the, in the case of something like GBA, we'll get a correlation between our brain delivery and the CSF delivery, which we think should be translatable to humans. But we won't know for sure until we get to the human experiment.

Yes, I agree with that. We won't know for sure until we do the human proof of biology trials. I think your question, Phil, was about whether or not we can rely on the biomarker readouts that we're getting from the NHP studies. And I think we can, in large part, I mean, for these kinds of things, we need to use larger animals, using rodents can be a fooler because the distances, the volumes just don't match up very well. But nonhuman primates because of their larger size, the dimensions are relatively similar to volumes of, for example, CSF space, brain approximate the human better than mice. But there's nothing like a real human experiment to be absolutely sure, as Todd said.

Our next question comes from Yanan Zhu with Wells Fargo.

This is Kuan-Hung for Yanan. I have 2 questions, one on receptor, you identifying one on the capsid. So first on the receptor. Can you share like how consistently the receptor you identified expressed among individuals? And do you know what factors may affect the expression levels of the receptor? And second, on the capsid. So after your partner exercised the option, do you further optimize the capsid for them or they just use the capsids that are already available in your library?

So on the receptor, I'm going to ask Todd to answer that and then later, I'll ask Pete to answer the question about the capsids.

For receptor responsible for the BBB penetration, in terms of the delivery, what we're seeing in animal models and the nonhuman primates and rodents, we're seeing expression in those species. We know it's expressed in human beings. We don't have readouts yet on variability amongst different humans. We do know that it's expressed and expressed in the endothelial cells and in the CNS of humans as it is in the animal model species as well. So we're focused on those aspects and the ability of it to the human receptor to transduce and improve BBB penetration in our models as well.

Yes. I mean, maybe I could just add. I mean I think you're asking a second order question, which is a really interesting question, which I think relates to individual variability within the species. And that's a second order question, and we'll get there. But we don't know the answer to that yet. And then with respect to the second question, I was going to ask Pete to talk about it because it relates to the actual agreement, I think, between the companies. And my understanding is that after they choose a capsid, they have up to 2 years to switch out to another capsid. So as we iterate and develop more and more sort of second and third-generation capsids, they will, of course, we share the data with them and they have the option to choose a newer one, which may be a more fit with their purposes. So that's how the deal was structured to my knowledge. Pete?

No, Al, I think you've captured it quite well with regards to the way the deals were actually structured themselves.

Our next question comes from Laura Chico with Wedbush.

First one, I see a recently released final CNS gene therapy guidance. Just curious if there was anything that stood out to you relative to the prior draft guidance or any impact to how you're thinking about development campaigns?

And then second, you mentioned the cash runway and some of the flexibility there around potential milestone payments. But I'm wondering kind of what sort of upper bound does that provide you in cash runway? Or are there other levers that you can pull besides the milestones to extend runway?

Thanks, Laura. I'm going to ask Pete to answer the question about the cash runway. But before that, Todd, any thoughts on the new guidance?

So I think what we're seeing and what we've seen over the past several years is particularly in the past couple of the consistent themes from the field in general and with the FDA. Very interested about and concerned about safety in terms of making sure that the therapeutic window. I think that there's also the insight from the FDA that they're very encouraged by the progress that's been made in the field. And so they've helped to outline ways of moving forward by identifying the path into the clinic for gene therapies. And so we're very excited by the guidance and the collaborative spirit of the FDA in moving these kinds of programs forward.

So Laura, with regards to your second question with regards to cash runway, I think Al characterized basically our balance sheet position quite well in his opening remarks. We believe the company is well capitalized with regards to where we're at. As we noted in our kind of third quarter operating results, the Pfizer monies were not included in the $132 million that were on our balance sheet as of close of 9/30. We believe that those additional Pfizer monies in addition to potential reimbursements associated with Neurocrine and other potential milestones that could come downstream specifically associated with the Novartis option agreement, which comes due in March of next year, it could potentially extend the cash runway as you were alluding to. Aas we've described to the Street, the Novartis option, they do have an option on 3 separate capsid programs. Each and every one of those programs actually would come with a trigger of $12.5 million per each option. So that could be a total of $37.5 million. We believe that potentially those could be struck, although we're not guiding to any of those at this time. And in addition to that $37.5 million, Novartis also has the option to take on 2 additional capsid options as well. So those could be for an additional $18 million per each of those options. So that's a total of $36 million. Again, at this time, we're not guiding with regards to where that's going to go. We believe all those things could potentially extend the cash runway of the organization. As we guided in the quarter, we still believe that we've got fair cash runway to take us into 2024. And I do believe Al earlier on also alluded to that we're having some ongoing conversations with regards to business development opportunities. All of those things could potentially add to the cash runway as well. I do want to highlight for all the analysts that are on the call today, we did put up a new shelf today as well as an ATM. Our existing shelf and ATM were actually expiring effective December 2 of this year. We feel like it's always good and prudent to make sure that you have a current shelf in place as well as an ATM. I think that's normal operating procedure for biotech companies these days. And again, all of those things could help us as we think about the future of the business and financing in the organization.

That's super helpful, Pete. Maybe if I could sneak one more in then. Just how should we be thinking directionally about R&D expense in '23 relative to '22? Still early stages, but kind of ramping up some efforts. So any clarity there?

Yes, that's a good question. I think you can most probably see from our operating results for the first 9 months of this year that we're basically on a trajectory to kind of close this year somewhere between, call it, USD75 million and USD80 million and basically operating burn for fiscal '22. I think as we think forward towards '23, we don't provide definitive guidance with regards to '23 operating burn. But I do think the one thing I could say to the Street is that we're going to be very mindful of our cash runway and our burn. And I think we're going to be very prudent with regards to our capital investment. So for now, at least to start next year, I think we can think about '23 kind of following suit with '22. But again, no specific guidance there.

Our next question comes from Yun Zhong with BTIG.

Detargeting built into the TRACER platform, please? And one question is how important is the And one question is how important is DRG de-targeting for IV if you are sticking to IV approach?

This is Al. I think it's very important. I think there's precedents for IV delivered capsids to produce DRG toxicity. And so we do think it's important and it's an important attribute of the capsids that we've identified so far that while they increase tropism and delivery into the CNS, we see de-targeting with some of these capsids off the dorsal root ganglion, exactly what we would want is increased transduction in the cells that we want to transduce and less in the cells that we'd rather not. And I would point out that DRG toxicity does seem to be expression related. And so I think it's great that we have some capsids that de-target dorsal root ganglion neurons.

Okay. So another question is, I believe you started from AAV9 given the maybe potency in crossing the blood-brain barrier, but you added AAV5. And is the main reason the advantage of in terms of preexisting neutralizing antibody. And also on preexisting neutralizing anybody, is the level normally consistent across wild-type capsid and the variant that you identified through the TRACER platform, please?

Yes. No, that's a great question. So we actually did use both AAV9 and AAV5 as our starting capsids for the TRACER platform. And you're right. The reason why we added AAV5, AAV9 is the sort of the king of neurotrophic capsids. So we wanted to improve on the very best ones that we have. AAV5 has the attribute that there's many fewer patients that have preexisting antibodies. So the numbers of patients which we can treat increases quite substantially by using AAV5 capsid. Your question about the immunogenicity of novel capsids, we can actually test that too. We have access to to patients' sera and the antibodies that are preexisting and we can test whether our novel capsids have more or less immunogenicity relative to their parent capsid. Todd, do you want to add anything?

Everything Al said. I'll add that with the changes that we're making to the AAV capsid, the AAV9 and AAV5 in this case, we don't expect there to be specific alterations in the neutralization activity in the population with those particular families. We are excited by the prospects though that TRACER could be our platform for identifying these novel capsids can also be deployed to identify capsids with less pre-existing neutralization activity. And so we're looking forward to that work in the future and are moving forward with our capsid platform.

Our next question comes from Dane Leone with Raymond James.

And congrats on all the progress. So somewhat in the similar vein of questions, but I'll ask it kind of a different way, which I think might be helpful. There is an interesting aspect of the work on Onasemnogene abeparvovec, where you had 2 patients that unfortunately passed away, and they were able to be evaluated for vector DNA and also the protein expression of the SMN protein by different organs. When you're optimizing these capsids and what you're trying to predict of the biodistribution and the tropism, I guess there's a couple of angles here. I mean do you think there's really an ability to dial in where the vector DNA is localizing, obviously, in the case of Onasemnogene, there was a lot in the liver, which created some of the toxicity management that happened, but there was also vector DNA across pretty much all of the major organs. Although the SMN protein really was more localized in expression around the spinal motor neurons. So I guess there's like kind of 2 things here. Like how much can you actually dial in where the vector DNA was hanging out and potentially creating some toxicity versus the actual protein expression of the vector?

Yes. No, that's central to a lot of what we're thinking about in terms of safety. And so the great thing about our capsids is is that it can help us with delivery of DNA to various cells, right? And that's why we're excited by the de-targeting data that we have. And we can look at both messenger RNA in those cells as well as DNA. And we actually look at DNA, mRNA and protein when we get to the point of choosing capsids. So we can look at all 3. And as you point out, some of the toxicity is expression related. And some may be SMN protein expression related as pointed out by the paper from Colombia a few years ago. Some it may not be expression related. Some may be simply immunogenicity versus the capsid and perhaps other ways that gene therapy can be toxic. So we have to consider all these potential avenues by which toxicity can be displayed. I think having novel capsids derived from TRACER that can de-target organs is very helpful. And if we combine that with promoter selection, we can certainly really fine-tune expression to a level that is potentially unprecedented. And so Todd, do you have anything to add to that?

I think one of the key aspects is the mRNA-based readout from the TRACER platform. And so we're not just looking at DNA delivery, what's making us successful with the TRACER platform is we really hone in on that mRNA expression level in addition to the DNA delivery. So we look at multiple tissues, all the tissue, you would imagine and probably some more when we evaluate our capsid and build our capsid profiles for different indications. And so we really do try to build that profile and to identify the capsid that fits the profile and give us the therapeutic window we need.

The other component is there a couple of different ways when we think about targeting a particular tissue or cell type and de-targeting others. One is literally we get more in where we want it and we get less in where we don't want it. The other context is if we can improve the potency getting to the target tissue, then we can lower the dose, which also, in and of itself reduces the delivery to our off-target tissues. And so we have both of those opportunities in our TRACER platform.

Our next question comes from Sumant Kulkarni with Canaccord Genuity.

Just a specific one on the novel cell surface receptor that you have identified. Clearly, there appear to be some advantages related to CNS biodistribution. But are there any specific already known downside with capsid binding to that specific receptor?

Not quite... I'm not sure I understood the second sentence. Can you repeat the second part of your question...

I mean utilizing this receptor to get the response that you need, are there any kind of toxicity downsides or anything like that that are already known and how much you'd be able to manage around that?

So I think the question was, is there anything known about this receptor that we would potentially even need to manage around? Is that the question?

Yes, exactly.

Yes. Yes. So right now, we don't know anything that we would need to manage around. So I'll just leave it at that.

Our next question comes from Jack Allen with Baird.

I know it's hard to comment for your partners. But as it relates to getting proof-of-concept data, I'd love to hear any thoughts you may have as it relates to the potential progress at Pfizer's programs and any programs that are opted in by Novartis as well, the timing of those candidates moving to the clinic potentially...

Yes, Jack. So I wish I could tell you. They're the lead for these programs. And I'm sure they'll tell us all of us when the time is right and when they get more specificity around the time lines. But we can be relatively specific about our own plans. But we're going to have to let our partners be specific about theirs.

Okay. And then just one brief follow-up. Al, I know you've been really close with the Alzheimer space. Pete has around the corner here, and I think there's going to be some interesting beta amyloid data that's expected. I guess, generally, does the beta amyloid development have any impact on your plans for the tau antibody. I'd love to hear your thoughts.

That's a good question. So I do think that I've only read the press release from Biogen, and it does sound like very exciting times for Alzheimer's disease treatments. I think personally, I think we're on the dawn of new treatments for Alzheimer's disease, which I think is very welcomed because certainly, the patients need something more than the currently available therapy. So how it impacts our anti-tau program? What I would note is that in the field of Alzheimer's disease R&D, there's always been learnings from previous studies that we use. And the field has benefited from both failures and successes in the past. And so I'm looking forward to seeing the data at CTAD in a few weeks. And I'm sure there'll be learnings from that, that we will incorporate into our own program.

Thank you. I'm showing no further questions at this time. I'd now like to turn it back to Dr. Al Sandrock for closing remarks.

Well, I just wanted to say thank you, everyone, for joining us and for asking us some very interesting and important questions. Appreciate you being on the call.

Thank you for your participation in today's conference. This concludes the program. You may now disconnect.