Voyager Therapeutics Inc (VYGR) 2023 Q1 法說會逐字稿

Good morning, and welcome to Voyager Therapeutics First Quarter 2023 Conference Call. (Operator Instructions) Please be advised that this 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 completion of this call.

I would now like to turn the call over to Peter Pfreundschuh, Chief Financial Officer. Please go ahead.

Thank you, and good morning. Joining me on the call today are Dr. Al Sandrock, CEO; and Dr. Todd Carter, our Chief Scientific Officer. We issued our Q1 2023 financial results press release this morning. The press release and 10-Q are available on our website. We plan to provide a brief summary of key highlights from the quarter and reserve the majority of time for Q&A. In a moment, I will turn the call over to Al.

Before I do this, I want to remind everyone that during this call, Voyager representatives may make forward-looking statements, as noted in Slide 2 of today's deck. These forward-looking statements include future expectations, plans and prospects. All forward-looking statements are inherently uncertain and are 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 the various material risks and uncertainties based on the company as described in the company's most recent annual report on Form 10-K filed with the SEC. As of the filing of today's quarterly report on Form 10-Q, there have been no material changes to the risk factors described in our annual report. All SEC filings are available on the company's website.

Now it's my pleasure to turn the call over to Al.

Thank you, Pete, and good morning, everyone. Please turn to Slide 3. I'd like to take a moment to recognize the incredible innovation happening right now in Neurotherapeutics and in gene therapy. We believe we are witnessing a renaissance in Neurotherapeutics. Just this year, the second disease-modifying therapy for Alzheimer's disease received accelerated approval and the first drug was approved for Friedreich's Ataxia.

We've seen breakthroughs in treating negative symptoms of schizophrenia, something for which there are no approved therapies. Just 2 weeks ago, the FDA granted accelerated approval to an antisense oligonucleotide for SOD1 Amyotrophic Lateral Sclerosis. Importantly, the FDA baked the approval on the finding the treatment-driven reductions in neurofilament are reasonably likely to predict clinical benefit in SOD1 ALS patients, establishing a precedent for a biomarker-based path to accelerated approval.

I hope this will drive further new treatments for patients suffering from this devastating disease. At the same time, the gene therapy field is coming of age. We have recently seen the FDA approval of the first gene therapy for hemophilia B. Gene therapies offering important potential advances in treating Duchenne's muscular dystrophy and hemophilia A are approaching PDUFA dates. And through that, we may see the accelerated approval path utilized for a gene therapy.

Importantly, long-term data on Zolgensma, one of the first gene therapies approved, recently demonstrated durability of effect after 7.5 years, which physicians have called transformational.

Voyager sits at the intersection of Neurotherapeutics and gene therapy, and we believe we are uniquely positioned to leverage the advancements in both fields. To date, the delivery of gene therapies into the central nervous system has proven challenging. Approaches to inject these therapies into the brain parenchyma or various CSF spaces have not been very successful.

Voyager's tracer capsid discovery platform is the foundation of our approach to solving this delivery challenge. Voyager scientists have engineered multiple capsid libraries, each with more than 20 million novel variants of AAV9 and AAV5 capsids to select those novel capsids that display greatly increased transduction in the central nervous system following intravenous delivery.

We have leveraged these capsids to advance our own and our partners' CNS gene therapy programs, several of which are now advancing towards clinical trials. This is how Voyager is enabling the future of neurogenetic medicines and from where I see, it's an incredibly exciting place to be.

Moving to Slide 4, I will briefly review our investment rationale. Our first pillar of value is our tracer capsid discovery platform, which I just discussed. In the preclinical studies, our novel capsids delivered intravenously have demonstrated more than 100-fold higher transduction expression in the brain compared to conventional AAV9 capsids.

We have shown high levels of CNS gene expression at low doses, and we have demonstrated the ability to target specific cells such as neurons or glial, while they targeting the liver and dorsal root ganglia cells. We look forward to sharing more data on our capsids at ASGCT later this month.

Our second pillar of value is our CNS pipeline. We are advancing 4 programs through late research towards R&D. Two of these programs are wholly owned, our humanized anti tower antibody for Alzheimer's disease and SOD1 gene therapy program for ALS. The other 2 are; GBA1 gene therapy program for Parkinson's disease and our FXN gene therapy program for free drive ataxia are being codeveloped with Neurocrine.

Our third pillar of value is partnerships. We completed capsid option and license agreements with Pfizer and Novartis. We've executed strategic collaborations around our pipeline programs with Neurocrine, and we are exploring more such transactions.

Turning to Slide 5. We continue to make progress advancing our CNS pipeline. I'll note a few recent highlights. During the first quarter, we selected a lead humanized anti-Tau antibody candidate, VY-TAU01 for the treatment of Alzheimer's disease. In March, we presented new data at the ADPD meeting, highlighting the differentiating characteristics of this lead candidate.

Last month, we received 3 IND written feedback from the FDA for VY-TAU1. Voyager continues to expect to initiate GLP toxicology studies this year to enable an IND filing in the first half of 2024. Another change this quarter was to the time line for our SOD1 ALS gene therapy program. Voyager previously said, we expected to identify a lead development candidate for this program in the first half of this year that has moved out to the second half of this year as we continue to evaluate data from this program to identify the optimal development candidate.

We intend to provide updated guidance on the IND time line once we select the development candidates. Given where we are today, we expect the IND to occur in mid-2025. Our frataxin gene therapy program for Friedreich's Ataxia and our GBA1 gene therapy program for Parkinson's disease and other GBA1 mediated diseases, both continues to advance in collaboration with Neurocrine. I'm pleased with the progress we are making here.

Additionally, during the first quarter, we launched 2 new early-stage gene therapy programs combining vectorized siRNAs with our novel intravenous tracer capsids. One combines 2 siRNAs to enable specific knockdown of mutant HTT and MSH 3 for the treatment of Huntington's disease. The other uses siRNA to reduce to expression in the brain for the treatment of Alzheimer's disease.

I'd like to now turn the call over to Pete Pfreundschuh to discuss our financial results for the quarter.

Thanks, Al. I will cover some key financial points on this call, and I refer you to our press release and 10-Q issued today for further details. Please turn to Slide 6.

We announced Q1 2023 collaboration revenue of $150.5 million, composed of $69.5 million from the 2023 Neurocrine collaboration agreement or the GBA1 program $79 million from the Novartis option exercises, and $2 million from the 2019 Neurocrine collaboration agreement activities.

Our R&D expense was $18.6 million, an increase of $4.2 million as compared to Q1 2022, driven by increased headcount, increased program-related R&D spend, and milestone fees and offset by decreased facility costs.

Our G&A expenses were $9 million for the first quarter of 2023 as compared to $7.7 million for the same period in 2022. The increase in G&A expenses was primarily a result of increased compensation costs, driven by headcount increases.

As a result of strong revenues in Q1 2023, the company had net income of $124 million, resulting largely from our collaboration revenues as well as increases of $1.8 million in other income due primarily to increased interest revenue from cash and marketable securities.

Regarding the balance sheet, Voyager reported $273.3 million in cash, cash equivalents, and marketable securities at the close of March 31, 2023. We also had a receivable at the close of Q1 2023 from the Novartis' $25 million option payment received in April. Together, this resulted in pro forma cash, cash equivalents, and marketable securities totaling $298.3 million for the close of the quarter.

Of note, deferred revenue increased by $18.7 million related primarily to the upcoming payment from Neurocrine allocated to the 3 new discovery programs of $74.4 million. Offset by the recognition of $54 million into revenue from the Novartis option exercise.

The company has a sound balance sheet enabled by our non-diluted collaboration revenues. We expect that our balance sheet plus expected reimbursements will be sufficient to meet our planned operating expenses and capital expenditures into 2025.

I will now turn the call back over to Al.

Thank you, Pete. Turning to Slide 7. As you can see, Voyager has had a productive start to 2023. We began the year by securing $175 million upfront payment in strategic collaboration with Neurocrine Biosciences, followed by Novartis' often decision on capsids to 2 neurologic disease targets triggering another $25 million payment. These transactions strengthened our balance sheet and enabled us to further advance our platform and pipeline.

As discussed, we selected a development candidate for our anti-tau antibody program for Alzheimer's disease. We aim to select a development candidate for the ALS SOD1 program later this year, and we launched 2 new early-stage gene therapy programs for Huntington's disease and Alzheimer's disease.

In addition, I'm thrilled to welcome George Scangos to our Board of Directors as we announced in our press release this morning. George is one of the most accomplished executives in the entire biotech industry, having served as CEO of Vir, Biogen, and Exelixis. His vast experience building biotech companies that deliver highly innovative therapies to patients while creating value for shareholders will be invaluable to us as we strive to develop Voyager into a leader in neurogenetic medicine.

Looking forward, we continue our work to break through the barriers constraining the field of gene therapy and neurology. We will continue to share the exciting data we are generating at scientific conferences, including at ASGCT later this month. Importantly, our pipeline advancement is leading towards what we as multiple opportunities for value creation.

As we look towards 2024 and 2025, we anticipate the potential for multiple IND filings across our wholly owned and collaborative and/or license programs. This translates into multiple opportunities to earn milestone payments and even more importantly, as clinical trials began several shots on goal to establish human proof of concept for our novel capsids.

Furthermore, there is potential to see early biomarker-based evidence of disease impact in some of these very difficult CNS indications. And of course, we continue to engage in active discussions with potential partners around our platform and pipeline.

In summary, it's been a great start to 2023. And as always, it is all due to the incredible Voyager team. I look forward to continuing our momentum throughout the year. With that, we're happy to take any questions you may have. Operator?

(Operator Instructions) The first question that I have today will be coming from Jay Olson of Oppenheimer.

Congrats on all the progress -- we're interested in the work you're doing on anti-Tau. You are advancing an anti-tau antibody and initiating a Tau knockdown chain therapy program and could potentially have a vectorized anti-tau antibody. Can you just talk about how you'll optimize the development strategy and prioritize all of your different Tau targeting modalities?

And then eventually, do you think that anti-tau therapies can be monotherapy? Or do you think they are best to be combined with anti-evasive therapies? And then finally, can you just talk about how you balance the trade-off of advancing your tau therapies independently versus seeking a partner.

Thanks, Jay. Those are great questions. So first of all, what we like about Tau is that we believe it's a very important and well-validated target for Alzheimer's disease. And because of that, we're taking multiple approaches against this target.

And so as you pointed out, we have an antibody against the C-terminal domain of Tau. The development strategy there is to move forward with the passive antibody first and see whether or not we get proof of concept. In other words, to see whether or not we can block the spread of Tau by looking at CAT scans.

We think this is very feasible, and we can do it with not that many patients over a 1-year period. If we obtain proof of concept, then we have a couple of choices there. One is we can continue to proceed with the antibody to Tau all the way through to approval and/or we can initiate a vectorized anti-tau antibody program. So that would be the sort of the crossroads that we will see there.

In addition, we have this vectorized to knockdown, which we think is an additional shot on against a very important target. And this will be different in the sense that it doesn't rely on antibodies binding to extracellular Tau. This approach is to decrease the expression of all forms of Tau, intracellular and extracellular, and we saw some preliminary evidence of that approach at the ADPD meeting with the Biogen Ionis antisense against tau, where they were able to see effects on tau.

So we think it's a very important target. We think having multiple approaches is helpful against this target. And we think we can obtain proof of concept pretty rapidly in the clinic, taking advantage of tau imaging. The final question relates to whether or not we're going to partner. And we're always talking to partners, and we're always open to anything. We could go to proof of concept by ourselves. We have the capability to do that, and I believe we have the resources to do that.

However, we're open to anything but ultimately, I can't imagine that we would go all the way to commercialization for a disease as large as Alzheimer's disease. So we will need to partner that program. The question is when, and we have some choices there.

Finally, your question about combination or monotherapy. I believe -- look, I think we just started the era of disease-modifying therapies for Alzheimer's disease with the approval -- accelerated approval of 2 anti-A beta antibodies. As we all know, the efficacy is modest in the 25% to 30% range on the CDR from the boxes.

We'd love to get better treatment effects. And one approach might be to combine with a tau-reducing approach, whether it's an antibody or a knockdown. And so I think that we're going to -- we are likely to test combination treatments because I think once tau spreading starts to occur, you may need to address tau independently separate from the anti-amyloid antibodies or in combination with them. So I hope that answers all your questions, Jay.

Our next question will be coming from Jack Allen.

Congratulations on all the progress. I wanted to stick with the tau game as well. And I wanted to ask Al, I'm sure you're aware of the Eli Lilly results from the recent study where they measure tau and stratified patients by tau. I was wondering if you had any early thoughts on the specific population within the Alzheimer's disease group that you looked enroll? And any comments you have around the differential effects. It seems like Eli Lilly saw in their higher versus intermediate tau cohorts?

Jack, that's a really interesting question. I look forward to seeing the data at a scientific conference. But from what I gather, the people who had to hire tau burden when they started the treatment had less of a treatment effect. And I think that underscores, I think, what I was just saying that we may need to combine with a tau approach, tau-targeted therapy.

And so in terms of the population, even -- when we get -- enroll patients with mild cognitive impairment, which is the earliest symptomatic disease. The disease is pretty far advanced in terms of molecular pathophysiology, right? I mean not only has amyloid been accumulating for up to 20 years and have reached essentially a maximum burden in the brain. We see tau has already started to progress in many of these patients. And so I think that the -- even when you do the combination, you're going to need to go to an early stage of patients, at least MCI and maybe even earlier.

Got it. Great. And then I was also wondering if you had any comments on the competitive landscape as it relates to tau and any other programs you're closely monitoring to see early proof of concept in this space?

Well, I think that there are a number of mid-domain targeted antibodies that are now approaching readouts from efficacy trials to my understanding. So that will be very interesting. In our hands, we had multiple mid-domain antibodies that we could have humanized ourselves. In our hands, they weren't as consistently effective in the spreading assay in the animal studies, where we take human pathological to inject them into the animals and look at the spread of pathological taus.

So we're very hopeful that our C-terminal antibody remains differentiated. But I think it'd be wonderful to see efficacy with the mid-domain antibodies. These Alzheimer's disease patients need something additional, I believe, in addition to the anti-amyloid therapies. Todd?

I just wanted to add that from our studies, at least in our preclinical models, it's pretty clear that the epitope matters quite a bit. So they are the main antibodies of our own at work, and there are mid-billion antibodies that don't work, our C-terminal antibody, as Al mentioned, gave us the most robust and the strongest effect. So I think that as we see these antibodies come through the clinic, it would be very informative for the whole field to learn, hopefully, what works and then maybe what does.

Great. Congratulations again on the progress.

Thanks, Jack.

Our next question will be coming from Phil Nadeau of TD Cowen.

Congratulations on the progress. A couple from us keeping on the tau theme. In terms of the Tau antibody that you've chosen as a development candidate, how does that antibody compare to the one that produced the data at AAIC 2022? Is it simply a humanized version of that prior antibody? Or are there any other changes?

Go ahead, Todd.

Sure. It's the -- so we have shown data on a number of antibodies. The data you're talking about from -- is included data from multiple panels of antibodies that hit different epitopes. The antibody we're taking forward is a humanized version of the lead antibody from that presentation.

So it's a humanized version of the antibody that produced the 71% to 74% declines in tau. Yes. Okay. That's helpful. And then second, on the GLP tox, it sounds like you're going to complete the GLP tox and be able to file an IND within a year. That strikes us faster than average. How can you get that done so quickly? Is that based on feedback from the FDA or just prior experience?

It's both, actually. And there have been other humanized antibodies against pathologic proteins. The tricky part here is that the target for the antibody is not expressed in wild-type animals, which is typically what's used in the tox species, right? So in order to look at our targeted toxicity, you have to look in animal models where that's the only place that you have the pathological tau as being expressed.

Those models -- the animals don't do well. They die prematurely because of the disease. And so you have to work within the limitations of that. So we do have experience with humanized antibodies against pathological proteins in the brain. And so we've drawn on that experience. But also, we have FDA feedback. And so our preclinical toxicology plan is based on both.

Great. And then one last housekeeping question for Peter. Peter, the $25 million milestone that was received in April, is that all going to be booked in Q2? Or is there going to be an amortized component?

So we, from a rev rec perspective, recorded debt, obviously, in Q1, but cash is in Q2. Keep that in the numbers.

Our next question will be coming from Yanan Zhu of Wells Fargo.

Perhaps a tau question and a SOD1 question. So for tau, how would you think about the criteria for success once you get the tau-antibody PET imaging data, given the findings of the Tau antisense, as you mentioned before. I'm guessing mainly if tau-reduction on PET is less potent, then if there's still a reason that the antibody approach can be a reasonable modality to be further pursued. I'll start when the question is, could you give more color on the delay for the nomination of the candidate? Is it more about payload or vector optimization or some other reasons?

Those are great questions. I'll take the first one and Todd will take the second one. On the tau well, first of all, the antisense oligonucleotides is injected intrathecal. And so -- and our antibody is an intravenous drug that we're going to inject every 4 weeks. So that's a pretty big difference right there in the mode of administration.

We will obviously compare to others that are showing data on tau. We do have a minimum product profile that takes into account our competition. And so we will move it forward if we have -- first of all, we have to have a statistically significant reduction in the spread of tau. And then we'll compare to competitors and see if there's a space for an additional treatment.

Just keeping in mind that the different modes of administration, the higher ease of use of an intravenous antibody. And the fact that I think there's room for more than one that had treatment. When I was a physician, I always like having multiple options for my patients. Todd?

Yes. So on Slide 1, as you know, have pointed out, the development candidate in therapy is the combination of a capsid and payload transgene. We're continuing to work and evaluate the transgenes and our capsids. Our capsids continue to perform very well. I cite anybody on the call to check out the ASGCT presentation next week. We have a couple of -- we have a symposium presentation and oral presentation and some posters on able acids. We're seeing quite reproducible results and continued performance across the modern area. What we're trying to do is identify the optimal payload with the optimal capsid to meet our candidate criteria. And we hope to do that in the back half of this year.

Our next question will be coming from Laura Chico of Wedbush.

I guess, staying on the tau theme, I wanted to ask with the upcoming reimbursement decision for the anti-amyloid antibodies? Is there any learnings there that can inform or perhaps change your development strategy for tau?

And then one for Pete. Can you just remind us, it's obviously been a big year in terms of milestones coming in, the potential for any remaining milestone payments in 2023.

Thanks, Laura. Yes, on the reimbursement question, that's a really important question, and we have a lot to learn, I think, as the year goes on this year. But I think, look, we have to be mindful of the total number of patients that are going to require treatment. And we don't want to do anything that will be unhelpful to society. We want to help patients, and we want to make sure patients have access to the drug. And so I think there's a lot for all of us to learn in the coming years. But I think you're pointing to the concept that if there's a combination treatment, as 2 drugs that have to be reimbursed. And so we'll have to take that into account.

Yes. And Laura, with regards to your second question. So we don't provide a lot of forward-looking guidance with regards to future milestones. I know we've shared publicly the milestones relative to all of our partnerships and relationships that we have in aggregate and kind of put some breakdown, but a lot of that's been redacted.

I can say it this way with regards to our existing relationships, there are some potential milestones that we could be getting in more of a near term, I would say it that way. But again, we don't guide specifically with regards to those. And so I think that's most probably where we would leave it for now.

Our next question will be coming from Joon Lee of Truist Securities.

For the Huntington's program, it's interesting that you're taking both an allele specific and non-allele specific approaches with SNP and MSH targeting. Can you elaborate a little bit on your strategy here? And do you plan to include multiple siRNAs in a single construct to address multiple SNPs? And would you also combine SNP as well as MSH in a single construct?

Yes. Thanks. I'll start and I'll ask Todd to finish the answer. So I would say that in some ways, both are kind of an allele-specific both targets because MSH3 targets the expansion, which only occurs off the mutant -- and obviously, the allele-specific mutant Huntington targets is an allele specific approach.

So in some ways, I look on it as both are kind of preserving both targets. By targeting both of these. We're preserving the expression of wild-type Huntington, which I think is the goal because I think there's a lot of concern that we need to preserve well-type Huntington expression. So -- and then yes, I mean I'll let Todd answer but our aim is to combine both as I factorized siRNA into the same vector. Todd?

Yes. So that's right, Al. So we do plan and incorporating both siRNAs. The payload for the siRNA is relatively small. So it's not a problem to fit multiple in a single vector. We can do a bicistronic approach. That said, I mean we could explore and evaluate them independently as well. So that's always an option we could choose to move forward with.

We plan on going after MSH3 pan manner, which would affect the mutant allele specifically. And then the approach to the allele-specific Huntington is a SNP-based approach to knock that down in all specific path.

So Joon, you're right that a SNP-based approach, we're not going to be able to treat every single Huntington's patient. We'll start with the most common alleles and then ultimately, we may need to do a second allele-specific MH mutant HTT program and so forth.

And I have a follow-up on the tau program. You have some -- people alluded to, you have multiple programs, multiple shots on goal. You have the approach to targeting extra cellar species as well as the intracellular species with the siRNA. Is there one species in your view, that is probably more important to address? Or I know you probably say both, but which one has more like evidence as the more dangerous or pathogenic for?

Well, I wish I nearly answered to that question. I think that's part of the complexity here is that there are multiple forms, if you will, of how in the extracellular space -- and it's pretty certain that targeting just the end terminal containing extracellular species of -- to probably doesn't work because the multiple approaches have been tried for those. But I think that I don't have an answer. Maybe, Todd, do you know what the pathologic species it?

No, I don't know. Yes. No. I mean…

So more along the lines, intracellular versus arose because your SRA approach the target, I believe, the interspecies preferentially.

Yes. Well, that actually will target both -- I mean it will target the synthesis of all forms of power. So if we decrease -- we will definitely increase interest value, which the antibody probably won't be able to do very much at all. But it will also -- it will also target extracellular tau because that's the source of extracellular tau is intracellular.

Would you say that the siRNA or percent would have a little bit higher progress success? Or is that still TBD?

Yes. But every approach is going to have its own benefit risk profile and mode of administration issues and things. So I think it's still too early to know to be certain which approach is going to be optimal for patients. But I think it's such an important target we wanted to go after it with multiple approaches.

Our next question will be coming from Sumant Kulkarni from Canaccord.

Nice to see all the progress that the company has a clear and exciting time to be targeting the specific conditions that you are. So I have a question on your SOD1 ALS gene therapy program. Now that 12% is available, how do you expect the landscape to change with respect to clinical trial recruitment? And is there any merit in running a specific preclinical model in combination with 12%?

Okay. I think I heard the first question, but I'll start and then I'm not sure I heard the second one. But I think the first question relates to the feasibility of recruiting patients in the setting of a person being approved. And I think there is -- first of all, it's wonderful that patients with a terrible disease have treatment options. So congratulations to Biogen and Ionis for getting that across the finish line.

For us, we could either take patients who are already on the person and see it to require and give them the gene therapy and see if the requirements for a person has decreased, perhaps to 0, but it could just be decreased. And we can track neurofilament as a marker to know whether or not the treatment is adequate, for example.

Another approach would be to go to untreated patients. There may be parts of the world where it's hard to access the person. And then a third approach would be to go very early even before symptoms to get rid of the toxic gain of function, autosomal dominant mutation. So those are the 3 approaches we're considering now. And time will tell which one of these is the best option.

But I think it's -- I think that the -- as I alluded to in my comments, the fact that neurofilament is considered, by regulators, at least FDA, as a validated surrogate outcome measure only helps in terms of making the development more feasible, I believe. And then you may have to repeat the second question because I'm not sure I heard it.

Sure. The second part of that was, is there any merit in running a specific preclinical model for your gene therapy in combination with 12% to optimize the product?

So the question was whether we're doing preclinical studies. So there are a couple of SOD1 transgenic mouse models, G93A, G37R, et cetera. We could add -- do the combination study in vivo. But I'm not certain that, that would be necessary before we did the study in patients. I think that we have a very good blood-based biomarkers that we can use to monitor patients in terms of the amount of injury to motor neurons. And some of these animal models, they're not very predictive of what happens in the clinic. So I worry about relying too much on these animal models.

The next question is coming from Jack Allen of Baird.

Great. I just wanted to reach out and see if you have any comments around the ability of Magnum primates. I know earlier this year, there was a ban of importation of these critical research assets. And I wanted to gauge your, I guess, awareness of this and any comments you have as it relates to your preclinical programs that you have ongoing?

Jack, it's Todd. So it's a great question. I think the entire field is watching very carefully. We certainly are watching the nonhuman primate availability quite closely.

To date, we have not been adversely affected by nonhuman primate availability. We set up agreements with multiple vendors to make sure we have options in case an issue should arise. And all I can say is that what we're doing our best to mitigate any risk and watching very closely.

This concludes today's Q&A session. There are no more questions in the queue. I would like to turn the call back over to Dr. Al Sandrock for closing remarks.

Thank you, everyone, for joining us today and for the great questions. Feel free to follow up with us directly if you have any further questions. Thanks again.

Thank you, everyone, for joining today's conference call. This concludes today's event. You may all disconnect, and everyone, have a great rest of your day.