Voyager Therapeutics, Inc. (NASDAQ:VYGR) Q3 2022 Earnings Call Transcript

Voyager Therapeutics, Inc. (NASDAQ:VYGR) Q3 2022 Earnings Call Transcript November 8, 2022

Voyager Therapeutics, Inc. beats earnings expectations. Reported EPS is $0.45, expectations were $-0.32.

Operator: Good morning, and welcome to Voyager Therapeutics Third Quarter 2022 Conference Call. All participants are now in a listen-only mode. There will be a question-and-answer session at the end of this call. 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 investor section of the company’s website approximately two hours after the conclusion of the call. I would now like to turn the call over to Peter Pfreundschuh, Chief Financial Officer.

Peter Pfreundschuh: 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 statement 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.

Alfred Sandrock: Thank you and Pete, and good morning, everyone. I would 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 has been constrained by delivery challenges. Gene therapy has been limited by narrow therapeutic windows and associated safety issues. Neurology is limited by the difficulty for getting larger molecules across the blood-brain-barrier. At Voyager, we are leveraging cutting edge expertise in capsid discovery, and deep neuro pharmacology capabilities to address these constraints, which we believe will ultimately create significant value for patients and shareholders.

We have created three pillars of value at Voyager. First, our TRACER capsids 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 displayed 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 trans-gene expression in the brain compared to conventional AAV9 capsids. We have also demonstrated blood-brain-barrier penetration across multiple species, including mice and non-human 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 a range of (Ph) 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 trial. 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 protein and oligonucleotide 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 is each of our three 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 capsids licenses are structured around this target, not the capsids. 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 tests and we may also select that tests for some of our own internal programs. The benefits of this structure are twofold. First, because these deals are not exclusive to the capsids, we have the optionality to continue to pursue partnerships. Second, some of our partners do choose capsid that we also utilize in our own programs, they may provide initial clinical validation of our capsids.

I want to dig a bit deeper into the pipeline now. Voyager continues to advance our three prioritized programs, as humanized anti-tau antibodies for Alzheimer’s disease, SOD1 gene silencing for AOS and GBA1 gene replacement for Parkinson’s disease. In addition to these three programs, I want to remind you that we have a collaboration ongoing with Neurocrine to develop a gene therapy for free 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 from 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 vein 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 of biology. Our therapeutic hypothesis is that 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 in 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 travel. We are on track with our work to humanize the murine antibodies. Moving now to GBA1 Parkinson’s disease up to 10% of Parkinson’s disease patients have a 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 benefits. GCase levels can be measured in CFS, as can 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 a GBA1 gene replacement with a CNS tropic BBB penetrant, novel TRACER derived capsids. NHB studies to select our lead candidate are underway. And now SOD1ALS. ALS is a rapidly progressing neurodegenerative disease that typically leads to death approximately three 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 , 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 constructs with a CNS-tropic blood-brain-barrier penetrance, novel TRACER derived capsids. NHP studies to select our lead candidates are underway. We continue to expect to identify lead development candidates for all three programs between Q4 2022 and H1 2023. These lead candidates will and be event with 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 with our ability to execute during the third quarter and the subsequent period. And the company is gaining momentum as we close 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 Peter Pfreundschuh as CFO and Tristan Morrison as Senior Vice President of Corporate Affairs. And we promoted Dr. Todd Carter to Chief Scientific Officer.

We also presented encouraging pre-clinical data at the AAIC and ESGCT Conferences. Those posters are on our website if you haven’t seen them. And we saw 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 pre-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 have been CEO of this company for about seven-months now and I’m so excited to be working with such incredibly talented scientists and other professionals. With that, we are happy to take any questions you may have. Joining me today for Q&A are Peter Pfreundschuh, our CFO and Dr. Todd Carter, our Chief Scientific Officer. Operator.

Q&A Session

Operator: Thank you. Our first question comes from Jack Allen with Baird. Please go ahead.

Jack Allen: Thank you so much for taking the questions, and 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 are 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 captive library of future capsids that you have for different assets? Love to hear any thoughts as it relates to that.

Alfred Sandrock: Thanks, Jack. This is Al, and I will start and I’m sure Paul 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.

Todd Carter: Yes. I think you captured it quite well.

Alfred Sandrock: Thanks, Todd.

Jack Allen: 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 then those conversations seem to have been going on for quite a bit. I would 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?

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

Jack Allen: Great. I will jump back in the queue. Thanks so much for the questions.

Operator: Thank you. One moment for our next question. Our next question comes from Phil Nadeau with Cowen. Please go ahead.

Philip Nadeau: Good morning. Thanks for taking our questions. A follow-up on the selection of the lead candidate in – with the GBA1 and SOD1 therapies. Can you talk a bit more about what measures you are able to capture in the non-human primates to select between candidates? Is it simply a transcription of certain brain areas and safety or are there biomarkers and other measures that will inform your decision?

Alfred Sandrock: Todd, do you want to take that?

Todd Carter: Sure. So yes, the answer to your question is we are looking at a number of things. So when we go in 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 are looking not only where the vector goes, the level of – in the case of GBA, key case activity, the protein, the enzymatic activity. In the case of SOD1, ALS program, the amount of knockdown we achieved in the relevant frame regions. We also look at where we hope to not go. So the off-target issues that Al mentioned earlier when they will get capsids. So when you look at all of those components. In addition for something like the GBA, we can look in the fluid compartment such as the cerebral spinal fluid for delivery into that space, as a marker and a correlate for how much transduction or delivery we get it to the brain. And that is something that we are hoping to use as we move forward in this clinic as well.

Philip Nadeau: And just one follow-up. In your experience, how predictive is the NHP model of what happens? I appreciate it is probably the best model that we have. How much uncertainty remains after you see these measures in NHP?

Todd Carter: So for our novel capsids, They are novel capsids. We have identified a receptor for one capsids family, which we think gives us increased translatability in the human. 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 will get a correlation between our brain delivery and CSF delivery, which we think should be translatable to humans. But we won’t know for sure until we get to the human experiment.

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

Philip Nadeau: That is very helpful. Thanks for taking that questions.

Operator: Thank you. One moment for our next question. Our next question comes from Yanan Zhu with Wells Fargo. Please go ahead.

Unidentified Analyst: Hello, thanks for taking our question. This is (Ph) for Yanan. I have two questions, one on receptor, you identifying one on the capsids. So first on the receptor, can you share like how consistently the receptor you identify express among individuals and do you know what factors may affect the expression levels of the receptor? And second on the capsids. So after your partner exercise the option, do you further optimize the capsids for them or they just use the capsids that are already available in your library? Thank you.

Alfred Sandrock: So on the receptor, I’m going to ask Todd to answer that, and then later I will ask Pete to answer the question about the capsids.

Todd Carter: The receptor is responsible for the BBB penetration in terms of the delivery, what we are seeing in animal models and the animal primates and rodents we are seeing expression in those species. We know it is expressed human beings. We don’t have readouts yet on variability amongst different humans. We do know that it is 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 are focused on those aspects and the ability of it to the human receptor to transduce and improve BBB penetration in our models as well.

Alfred Sandrock: Yes. I mean, maybe I could just add, I mean, I think, you are asking a second order question which is a really interesting question, which I think relates to individual variability within a species. And that is a second order question and we will 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 two years to switch out to another capsid. So as we iterate, and develop more and more sort of second third generation capsids, they will – of course we share that data with them and they have the option to choose a newer one, which may more fit their purposes. So that is how the deal was structured to my knowledge. Pete.

Peter Pfreundschuh: Al, I think you have captured it quite well with regards to the way that deals were actually structured themselves.

Unidentified Analyst: Got it. Thank you so much.

Operator: Thank you. One moment for our next question. Our next question comes from Laura Chico with Wedbush. Please go ahead.

Laura Chico: Hey, good morning guys. Thanks for taking the questions. First one, actually you recently release final CNS gene therapy guidance. Just curious if there was anything that stood out to you relative to the prior draft guidance for any impact to how you are thinking about development campaigns? And then second, you mentioned the cash runway and some of the possibility there around potential milestone payments. But I’m wondering kind of what sort of upper bound does that provide you in cash runway or is there other levers that you can pull besides the milestones to the extent runway? Thanks very much.

Alfred Sandrock: Thanks, Laura. I’m going to ask Pete and to the question about the cash runway. But before that, Todd, any thoughts on the new guidance.

Todd Carter: So I think what we are seeing and what we have seen over the past several years is particularly in the past couple, the consistent theme 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 is also the insight from the FDA that they are very encouraged by the progress that has been made in the field. And so they have helped to outline ways of moving forward of identifying the path into the clinic for gene therapies. And so we are very excited by the guidance and the collaborative spirit of the FDA in moving these kinds of programs forward.

Peter Pfreundschuh: Yes. So Laura, with regards to your second question, with regards 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 are at. As we noted in our kind of third quarter operating results of 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 to in March of next year, but you could potentially extend the cash runway as you were alluding to.

As we have described to the Street, the Novartis option, they do have an option on three separate capsids programs. Each and every one of those programs actually would come with a trigger of $12.5 million for each option. So that could be a total of $37.5 million. We believe that potentially those could be struck, although we are not guiding to any of those at this time. And in addition to that $37.5 million Voyager also has the option to take on two additional capsid options as well. So those could be for an additional $18 million for each of those options, so that is a total of $36 million. Again, at this time, we are not guiding with regards to where that is 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 have got a fair cash runway to take us into 2024. And I do believe Al, earlier on also alluded to that we are 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 ATM were actually expiring in December 2nd of this year. We feel like it is always good and prudent to make sure that you have a current shelve in place as well as an ATM. I think that is normal operating procedure for biopsy companies these days. And again, all of those things could help us as we think about future of the business and finance from the organization.

Laura Chico: That is super helpful, Pete. Maybe if I could sneak one more and then just how should we be thinking directionally about R&D expense in 2023 relative to 2022 still early stages, but kind of ramping up some efforts. So any clarity there? Thanks.

Peter Pfreundschuh: Yes, that is a good question. I think you can most probably see from our operating results for the first time this year that we are basically on a trajectory to kind of close this year somewhere between call it $75 million and $80 million, basically operating burn for fiscal 2022. I think as we think forward towards 2023, we don’t provide definitive guidance with regards to 2023 operating burn. But I do think the one thing I could say to the street is that, we are going to be very mindful of our cash runway and our burn. I think we are 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 2023 kind of following suit with 2023, but again no specific guidance there.

Laura Chico: Got it. Thank you very much guys.

Operator: Thank you. One moment for our next question. Our next question comes from Yung Zhong with BTIG. Please go ahead.

Yung Zhong: Okay, great. Thank you very much for taking the question. And so our liver and DRG toxicity – sorry, de-targeting built into the capsid, sorry. The TRACER platform, please. And one question is how important is DRG de-targeting for IV if you are sticking to IV approach?

Alfred Sandrock: This is Al. I think it is very important. I think there is precedence for IV delivered capsids to produce DRG toxicity. And so we do think it is important attribute of the capsids that we have identified so far that, while they increased tropism and delivery into the CNS. We see de-targeting with some of these capsids of the door. So we are getting exactly what we would want this increased transduction in the cells that we want to transduce than less in the cells that we would rather not. And I would point out that DRG toxicity does seem to be expression related. And so I think it is great that we have some capsids that de target dorsal root ganglion neurons.

Yung Zhong: Okay. So another question is I believe you started fromAAV9 given the maybe potency in crossing the blood-brain-barrier. But you AAV5 and is the main reason the advantage of in terms of pre-existing neutralizing antibody and also pre-existing neutralizing anybody, is the level normally consistent across wall type capsids and the variant that you identify through the TRACER platform, please? Thank you.

Alfred Sandrock: Yes. No that is a great question. So we actually did use both AAV9 and AAV5 as our starting capsids for the TRACER platform. And you are right, the reason why we added AAV5, AAV9 is the sort of the king of neurotropic capsids. So we wanted to improve on the very best one that we have. AAV5 has the attribute that there is many fewer patients that have pre-existing antibodies. So the numbers of patients we can treat increases quite substantially by using AAV5 capsids. And we can actually – your question about the immunogenicity of novel capsids, we can actually test that too. We have access to patients – and the antibodies that are pre-existing and we can test whether our novel capsids have more or less immunogenicity relative to their parent capsids. Todd, you want to add anything?

Todd Carter: Yes. Thanks Al. Everything Al said, I will add that with the changes that we are making to the, AVV capsids, AVV9 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 prospect, 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 are looking forward to that work in the future and are moving forward with our capsids platform.

Yung Zhong: Great. Thank you very much.

Operator: Thank you. One moment for our next question. Our next question comes from Dane Leone with Raymond James. Please go ahead.

Dane Leone: Hi thanks for taking my questions and congrats on all the progress. So somewhat in the similar vein of questions, but I will ask it kind of a different way, which I think might be helpful. There was an interesting aspect of the work on a SMN1 gene – where you had two 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 are optimizing these capsids and what you are trying to predict of the biodistribution and the trophism. I guess there is a couple angles here. I mean, do you think there is really an ability to dial in where the vector DNA is localizing? Obviously in the case of on SMN1 gene there was a lot in the liver which created a some of the toxicity management that happened.

But there was also vector DNA across pretty much all the major organs. Although the SMN protein really was more localized, in expression around the spinal motor neurons. So I guess there is like kind of two things here, like how much can you actually dial in where the sector DNA is hanging out and potentially train some toxicity versus the actual protein expression of the vector?

Alfred Sandrock: Yes. No, that is central to a lot of what we are thinking about in terms of safety. And so the great thing about our capsids that it can help us with delivery of DNA to various cells. And that is why we are 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 capsid. So we can look at all three. And as you pointed out, some of the toxicity is expression related, and some may be SMN protein expression related as pointed out by the paper from Columbia a few years ago. Some 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 be 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?

Todd Carter: I think one of the key aspects is the mRNA based readout from the TRACER platform. And so we are not just looking at DNA delivery, what is 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 caps profiles for different indications. And so we really do try to build that profile and to identify the capsid that fits profile and give us the therapeutic window we need. The other component is, there are 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.

Dane Leone: Thank you.

Operator: Thank you. One moment for our next question. Our next question comes from Sumant Kulkarni with Canaccord Genuity. Please go ahead.

Sumant Kulkarni: Good morning. Thanks for taking my question. Just a specific one on the novel cell surface chip that you have identified. Clearly, there appear to be some advantages related to CNS bio-distribution. But are there any specific already known downsides to capsid binding to that specific receptor?

Alfred Sandrock: Not quite – I’m not sure I understood the second sentence. Can you repeat the second part of your question?

Sumant Kulkarni: 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 might you be able to manage around that?

Alfred Sandrock: 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?

Sumant Kulkarni: Yes, exactly.

Alfred Sandrock: Yes. So right now, we don’t know of anything that we would need to manage around. So I will just leave it at that.

Sumant Kulkarni: Got it. Thank you.

Operator: Thank you. One moment for our next question. Our next question comes from Jack Allen with Baird. Please go ahead.

Jack Allen: Thank you so much for taking the follow-up. I know it is hard to comment for your partners, but as it relates to getting proof-of-concept data I would love to hear any thoughts you may have. Is it related 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?

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

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

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

Jack Allen: Okay. Thanks so much for taking the follow ups.

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

Alfred Sandrock: 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.

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