Voyager Therapeutics, Inc.
Q3 2018 Earnings Call Transcript

Published: 8 Nov 2018

[Operator:]

Good afternoon, and welcome to the Voyager Therapeutics Third Quarter 2018 Financial Results and Corporate Highlights Conference Call. At this time all participants are in a listen-only mode. Following the formal remarks, we will open up the call for your questions. Please be advised that this call is being recorded at the company’s request. At this time, I'd like to turn it over to Matt Osborne, Voyager's Vice President of Corporate Affairs, Communications and Investor Relations. Please proceed.

[Matt Osborne:]

Thank you. Good afternoon, and welcome to the conference call. This afternoon, we issued a press release, which outlines the recent corporate highlights and financial results for the third quarter of 2018 and provides financial guidance for 2018. We also issued a separate press release providing an update on the longer-term clinical results with VY-AADC for Parkinson's disease. These releases are available at voyagertherapeutics.com. Today on our call, Andre Turenne, Voyager's President and CEO, will review our recent corporate and clinical program highlights; Dinah Sah, Voyager's Chief Scientific Officer will review updates with our pre-clinical pipeline program; and Allison Dorval, Voyager's Chief Financial Officer will review the financials; and then we will open up the call for your questions. Before we begin, just a reminder that various remarks we make during the call about the company's future expectations, plans and prospects constitute forward-looking statements for purposes of the safe harbor provisions under the Private Securities Litigation Reform Act of 1995. These forward-looking statements represent the company's view as of today, August 7, 2018. Voyager disclaims any obligation to update these statements to reflect future events or circumstances. Please refer to today's press release as well as Voyager's filings with the SEC for information concerning risk factors that could cause actual results to differ materially from those expressed or implied by such statements. With that, I'll pass the call over to Andre.

[Andre Turenne:]

Thank you, Matt, and good afternoon everyone. Thank you for joining us on the call. As we highlighted in today's press releases, the third quarter was a productive one for the company with positive new data on both our lead program, VY-AADC for Parkinson's disease, and on our pipeline programs. We described today in a separate press release the positive longer term results from the ongoing open-label dose escalating Phase 1b clinical trial of VY-AADC. At the latest timepoint measured for each of the five patient cohorts, patients and the two highest dose cohorts experienced mean, durable improvements in good ON time, which is ON time without troublesome dyskinesia of 1.7 hours per day at 18 months for Cohorts 3 and 2.7 hours per day at years for Cohorts 2. Importantly these improvements in good ON time were achieved with large and sustained reduction in daily oral levodopa and related medications in these two highest dose cohorts. This included a 43% reduction from baseline for Cohort 3 at 18 months and 21% reduction from baseline for Cohorts 2 at two years. Since we've selected a dose of up to 2.5 e12 vector genomes for the Phase 2, which is between the doses used in Cohorts 2 and 3 of the Phase 1b combining the data from the 10 patients in these two cohorts provide the most relevant dataset. For this combined group of 10 patients VY-AADC improved patient's good ON time by 2.4 hours per day at 12 months, which is the timepoint for the primary endpoint of the Phase 2 trial and 2.6 hours per day at 18 months, which is the latest timepoint measured for both Cohorts. We've learned from the Phase 1b that patients with severe dyskinesia baseline could be more challenging to treat as they may take longer to settle in with good ON time after administration of VY-AADC. We've also learned from the Phase 1b that the selection of patients for the study with sufficient off-time baseline may meaningfully enrich the patient population to show a clinically important restoration of motor function. We've incorporated these insights into the design of the Phase 2 trial. Of the 10 patients enrolled in cohorts two and three of the Phase 1 trial seven would have likely been eligible for the Phase 2 based on the more stringent criteria of minimum amount of off-time and less severe dyskinesia at baseline now incorporated into the study. For these seven patients the improvements and good on-time were an impressive 2.8 hours at 12 months and 2.5 hours at 18 months. Now it's worth taking a moment to characterize the potential clinical significance of these observed improvements. Great on-time is frequently used in Parkinson's clinical development and disease management. And by definition is the time that patients are on or responding to their medication, but without troublesome dyskinesia as recorded in a patient diary. The disease burden for these patients is just the opposite. It's the sum of the time per day when patients are off. That is stiff and immobile and not responding to their oral medications, plus the time that they are on, but with troublesome Dyskinesia or serious uncontrollable movement. These disease states are enormously problematic for these patients and as they become more frequent, prevents them from carrying out their normal lives. So for the 10 patients from cohorts two and three of the Phase 1b trial, this disease burden, again the sum of off-time and troublesome dyskinesia, was on average five and a half hours per day at baseline. Following treatment with VY-AADC, this was reduced by 46% at 12 months and by 47% at 18 months. With similar reductions observed in the seven of 10 patients who would have been eligible for the Phase 2 study. Again and importantly, these improvements were achieved, at the same time as patients at large and sustained reduction in their levodopa and related medications versus pre treatment. For the 10 patients in cohorts two and three and the seven among them who would have been eligible for the Phase 2, the sustained average reduction in levodopa equivalent doses were between 30% and 40% from baseline at both 18 months and 12 months. We expect to provide the next update from this Phase 1b trial, in Q2 2019, wants all 10 patients at the these two highest dose cohorts averaged two years since treatment. Also in Q2, 2019 we expect to announce 12-month results from all eight patients from an initial Phase 1b trial in which VY-AADC was administered via the Posterior Infusion Trajectory, which is the preferred surgical route of administration for the Phase 2 trial. Now turning to the regulatory update as previously announced in July 2018, we received written Type C meeting feedback from the FDA indicating that the results from the Phase 2 randomized, placebo-controlled trial, if it were to meet its primary endpoint and in the absence of major safety concerns, likely may be considered sufficient for submission of the BLA for review. In October 2018, we received an addendum from the FDA to the July 2018 written responses in which the FDA informed us that although the data from the Phase 2 trial may support the safety and efficacy of VY-AADC and could be considered in the BLA review, the FDA currently considers the Phase 2 trial as an early phase exploratory study. We plan to engage with the FDA to gain further clarity on their most recent responses, we have scheduled Type B meeting later this year and will continue to actively seek and incorporate FDA guidance through the additional mechanisms now available to us via our RMAT designation. Operationally on the VY-AADC, we've been focused on the initiation and execution of the Phase 2 trial. We’ve selected 24 leading neurosurgical and neurology sites for the study. We are at the stage of our RD approvals, site activation and patient screening. As the first randomized placebo-controlled study of VY-AADC, great care is being applied to ensuring the blinding process at the IRB level and to enabling the rigorous coordination of patient selection, screening and surgical scheduling among the related investigator sites. We expect several, additional, connected neurology, neuro surgical sites to become activated before year-end and expect to provide an update upon dosing of the first patient. Before turning the call over to Dinah, who will discuss the exciting developments with our preclinical programs, I want to highlight updates on Voyager’s management team. Today we announced the appointment of Allison Dorval as Chief Financial Officer from her previous position as Vice President of Finance. I'm very pleased at Allison serving this role. Since joining the company in June 2017, Allison has built and led a strong finance team. With her more than 20 years of experience in finance and accounting, I'm absolutely thrilled to have Allison contribute to Voyager’s growth in this new capacity. In addition, we've also made good progress on our search for a Chief Medical Officer. We expect to finalize our selection process and look forward to also announcing this appointment soon. With that I will now turn the call over to Dinah?

[Dinah Sah:]

Thanks Andre and good afternoon everyone. I'll spend the next few minutes describing some of the recent exciting preclinical data with our Huntington's disease program and our ALS program, targeting the SOD1 mutation. Before doing so, it's important to take a step back and understand our systematic approach to fully optimizing not only the payload or in these cases probably the microRNA cassettes, but for both programs, delivery of the vector as well. First on payload selection for AAV-RNAi program, we begin with the most potent RNAi sequences based on in vitro transfection experiments and then place these selected RNAi sequences within engineered primary microRNA cassettes for expression in AAV. Multiple studies have demonstrated that primary microRNA cassettes provide better precision and efficiency of processing than short hairpin RNAs. So we have chosen to use the primary microRNA cassettes in our RNAi platform. We screen a number of primary microRNA cassettes, RNAi sequences to select the most potent candidates in vitro. These are then tested head-to-head in the mouse for in vivo knockdown of the target. The top three or four sequences are finally tested in a lead selection study in the large mammals such as nonhuman primate for the selection of the clinical candidate. In the in vivo studies we not only access knockdown of the target, but also conduct deep sequencing to evaluate precision of processing and guide to passenger ratio. I recall that the guide strands to active drug whereas the passenger strand is just along for the ride, no intended pharmacological activity. The final selection is based on the most robust and potent pharmacology, in this case, knock down of the target, as well as most selective pharmacology. Our first RNAi program at Voyager with ALS, SOD1 program where we optimized this RNA platform mostly by optimizing the primary microRNA cassette sequences. During this, we have work after extensive screening of numerous natural and engineered primary microRNA cassettes. We identified a handful of top primary microRNA cassettes. For the HD program, we use these top primary microRNA cassettes in essentially a plug and play system, together with the most potent RNAi sequences targeting Huntington. And thereby we're able to go from target to candidate that is optimized primary microRNA in a much shorter period of time. Then for ALS SOD1. So there was substantial leverage learnings from advancing our AAV RNAi platform. For production of AAV RNAi vectors in the back of Seph9 [ph] system. We have also optimized our vector genome configurations using molecular engineering. This is another very important feature of our RNAi platform. Now trying to delivery in both the PD and HD programs. We use intraparenchymal infusion with MRI guidance. Well, therefore be able to leverage our substantial learnings from the PD program, including the surgical procedure trajectory, planning and device, and apply these learnings to the HD program for intraparenchymal infusion. And then the press release today, we announced progress with our 510(k) clearance of V-TAG, a real-time interoperative MRI compatible neural navigational device as an additional choice for neurosurgeons in the Parkinson's disease program. And importantly, this could also be used for Huntington's disease program as well as other programs. We leveraged the one-time delivery of these vectors in unique ways to target precisely areas of the brain and spinal cord and the relevant cell types within those regions that most prominently contribute to disease manifestations. For Huntington's disease, this resulted in significant reduction of Huntington gene expression and deeper tissues and outer layers of the brain of large animals and for SOD1 ALS. We achieved significant reduction of SOD1 gene expression throughout a large animal spinal cord, including importantly, almost complete reduction of SOD1 in cervical motor neurons. Specifically for Huntington's disease our novel delivery paradigm targets both the putamen and thalamus which leverages more extensive and preserve neuronal pathways to the cortex. Then delivery to the putamen alone. This can offer the potential of a one-time treatment with VY-HTT01 to address motor, cognitive, and behavioral disabilities associated with Huntington's disease. We also conducted a robust analyses including quantitative measurement in multiple tissue punches and in more than a 100,000 neurons captured by laser microdissection. In order to measure Huntington knock down. To demonstrate that we are in fact getting the right amount of knockdown in the right tissues and in the right cell types. Our optimized. delivery paradigm resulted in reduction of Huntington Messenger RNAi on average by 68% in the caudate 67% in the putamen, 73% of the thalamus and 32% in cortical neurons. In the context of potential therapeutic benefit to patients as well as competitive landscape for HD. These are very compelling results. For VY-SOD102, we chose to assess the mini-pig, which has a spinal cord similar in length and diameter to the human spinal cord. We felt that it was important in this large species to test the spread of the vector up and down the spinal cord. With non-human primates the spinal cord is two to three times shorter than that of a human. So gradients seen with interstitial lumbar dosing in non-human primates are anticipated to be further magnified in the longer human spinal cord. Therefore, we felt that it was important to assess the spread of our vector and the knockdown in spinal cord that more closely resembles the human spinal cord in size. Here with VY-SOD102, a novel delivery paradigm comprising a onetime intraparenchymal infusion directly to the cervical region of the spinal cord, significantly reduced SOD1 mRNA in the spinal cord on average by 70% and 50% in the cervical and thoracic regions, respectively; both of these regions being critical for respiratory function and 82% reduction of SOD1 near the side of cervical injection. This knocked down in these regions is particularly important as most patients with ALS die of respiratory failure. Therefore, suppressing the disease causing gene expression in this region that controls respiratory function could offer a tremendous clinical benefit. In addition, VY-SOD102 reduced SOD1 mRNA by 22% even in the lumbar region. So in summary, we are very excited by the robust reductions of disease causing gene expression that were achieved as part of our latest delivery optimization efforts, in both our Huntington's disease and ALS programs. These data in large animals support our progress towards initiating human studies for both programs during 2019. Now briefly turning to our Friedreich’s Ataxia program and AbbVie collaboration to vectorize a tau antibody for the treatment of Alzheimer's disease and other tauopathies. Our Friedreich’s Ataxia program continues to progress towards selecting elite candidate that comprises an optimal capsid promoter and for transgene. We are conducting further studies with potential candidates, which included novel capsid that when administer IV provides bio distribution to key tissues for the treatment of FAA, the dorsal root ganglion, heart and dentate nucleus, where it is most important to restore Friedreich's Ataxia for clinical benefit. Our AbbVie collaboration to vectorize a tau antibody for the treatment of Alzheimer's disease and other tauopathies also continues to make good progress. With that, I'll turn it over to Allison.

[Allison Dorval:]

Thanks, Diana. Good afternoon, everyone. Voyager reported a GAAP net loss of $20.3 million or $0.63 per share for the third quarter ended September 30, 2018, compared to a GAAP net loss of $23.3 million or $0.89 per share for the same period in 2017. Collaboration revenues of $2.1 million for the third quarter of 2018 compared to $1.1 million for the third quarter of 2017. This increase reflects the recognition of revenue related to research services performed under the AbbVie collaboration agreement announced in February and was offset by reductions in amounts recognized under the Sanofi Genzyme collaboration. These reductions related to lower research and development services revenue as well as the impact of adopting certain accounting rules related to our recognition methodology. Research and development expenses decreased to $16.6 million this quarter from $19.6 million in Q3 last year. This was primarily a result of higher manufacturing costs last year to support the VY-AADC clinical program. This reduction was offset by increases in personnel and facility costs to support the advancement of our clinical and preclinical program. General and administrative expenses of $6.6 million for the third quarter of 2018 increased from $4.9 million last year, primarily due to personnel and facility costs to support the advancement of our lead and pipeline program, our platform, and our manufacturing capabilities. We ended the quarter with cash, cash equivalents and marketable debt securities of $179.6 million. Based on our current operating plan, we expect to end 2018 with total cash, cash equivalents and marketable debt securities above the previously guided range of $125 million to $135 million. We continue to project the cash, cash equivalents and marketable securities to be sufficient to fund operating expenses and capital expenditure requirements into early 2020. With that, I’ll turn the call back to Andre.

[Andre Turenne:]

Thanks, Allison. And with that, operator we can now take questions.

[Operator:]

Thank you. [Operator Instructions] And our first question comes from Brian Skorney of Baird. Your line is now open.

[Brian Skorney:]

Hey, good afternoon guys. Thanks for taking the question. I just wanted to kind of dig in a little bit on the changing sort of the FDA body language here with the addendum. Was there any new data submitted between getting the minutes back from the Type C meeting and this addendum that would trigger this? And is there any way you could just 8-K, the meeting minutes on the addendum for us. So we have an idea of what the FDA is new change of a possession us.

[Andre Turenne:]

Yes, thanks for the question, Brian. So there are no new data between the Type C meeting and this addendum. And what we’re endeavoring to do next is to sign out more getting in touch with the agency and we have a Type B meeting scheduled between now and the end of the year. And we’re going to look to have access also through the channels, we have the RMAT designation. So as soon as we have greater clarity, we’re going to provide the update on this, but that’s the bat for us for next step is really to engage, continue to engage with the agency to clarify their latest comment.

[Operator:]

Thank you. And our next question comes from Laura Christianson of Cowen. Your line is now open.

[Laura Christianson:]

Hi, guys. Thanks for taking my question. My first one is just looking at the data you provided on the L-Dopa dose reduction. And particularly in cohort two at 24 months, I’m saying that there’s been a 21.2% reduction overall. I know previously, you had mentioned 34% at six months. So I’m just wondering if this changes your view of the long-term efficacy or whether the L-Dopa reductions were brought in initially and you anticipate the more gradual reductions will yield the same results?

[Andre Turenne:]

Yes, thanks, Laura for the question. So when we look at the all the cohorts and the data we have to date overtime. We see clearly that we have a both a sustained reduction in levodopa, but one also that’s a different cohort by cohort. So where we’re seeing the lease reduction is with Cohort 1 and then there is a good dose response here where a Court 2 the dose response in the levodopa equivalent dose remains a low versus baseline. And then that’s even more the case for the third cohort where we have the highest and most sustained reduction in the levodopa equivalent doses. So for us, again, having now made a dose selection of choice that we’re having a dose that in between Cohort 2 and Cohort 3, when we look at the relevant group, the cohort of 10 patients or to seven as we highlight in the comments in the press release that would likely be eligible for that Phase 2. We see a nice consistent reduction in levodopa equivalent doses. As you go through 12 months and 18 months, it stays in the 30% to 40% reduction versus baseline. So that’s quite significant because that goes to the core of the mechanism of this AADC replacement. So to be able to improve motor function, while at the same time the patients have this large and sustained reduction in the levodopa equivalent dose is towards the clear sign that the pharmacology is very active and what we’re seeing something sustainable.

[Laura Christianson:]

Got It. That’s helpful. And then just a quick one on the Phase 2, Phase 3, how consistent do you expect the dose concentration to be across patients in that trial with – the surgeon aiming for a concentration between Cohort 2 and Cohort 3, but potentially having some variability?

[Andre Turenne:]

Yes. So the concentration is fixed. The variability is going to come from the exact volume that’s delivered. That’s going to vary depending on the patient, every anatomy of the putamen is a little bit different patient by patient. So we expect the volume differences to be relatively small and therefore the total vector genomes delivered to the difference range to be relatively tight with this route of administration. This is a single infusion that’s required with a posterior route. And again, having the lot of the motor function in the posterior region of the putamen, the way to surgery will work is a works with that trajectory is that the most important area is impacted first and covered more totally with the infuse it. But to answer your question, we don’t expect a large variation in that volume and therefore in the vector genomes delivered.

[Laura Christianson:]

Perfect. That’s helpful. Thank you.

[Andre Turenne:]

You’re welcome.

[Operator:]

Thank you. [Operator Instructions] And our next question comes from Jeff Hung of Morgan Stanley. Your line is now open.

[Jeff Hung:]

Thanks for taking the questions. Can you provide some color on what the agency said, if anything during the Type C meeting regarding their thoughts on the Phase 2 being more exploratory?

[Andre Turenne:]

Yes. Thanks, Jeff. So as we reported after the Type C meeting – from our Type C meeting minutes responses to our question. The agency had responded to us that the Phase 2 alone likely maybe sufficient none of it would approved to be effective. To me it’s primary endpoint and to be safe for the submission of the BLA for submission. So that’s the feedback that we received at that time. And that’s why here we – we’re going to seek clarity on this addendum that we just received to be able to align with that agency on the next step. What’s clear that the Phase two, if the trial – that’s the right trial and this moving forward, what we’ll do once we have the benefit of getting greater clarity from the agency is that we’ll consider adjustments to the overall plans if necessary. So we can continue to be aligned with the guidance that they provide, once they clarified. But that’s where we stand right now. And again, we have the means of engaging with that agency having a Type B meeting in front of us and having access also again through the senior an accelerated type of engagement, we can get via the RMAT designation.

[Jeff Hung:]

And I think you just answered it, but maybe if I can push a little bit on that last part. So does the addendum change your base case assumption that the Phase 3 will be required regardless of the outcome of the Phase 2? When with the Phase 3 be sufficient for filing, or do you think additional studies will be required beyond your Phase 2 and Phase 3?

[Andre Turenne:]

Yes. So at this moment we won’t speculate on any changes to the plan. So we still believe that we have a robust plan with a Phase 2 and Phase 3 staggered design. And we’ll look to get the further dialogue with the agency to clarify. Again, any adjustments that – if any, that we make to the current plan. But the plan for the Phase 2, again, in terms of primary endpoint, in terms of the route of administration, the dose that we select in the patient population, the first placebo-controlled study for this therapy is absolutely what we believe is the right thing to do. So we’ll review with the agency, the plans in that totality via this therapy meeting and the other interactions we may have and we’ll provide updates as to the overall baggage in due time.

[Jeff Hung:]

Okay. And then maybe one last one. You’re excluding patients who are severely dyskinetic in the Phase 2. Can you remind us what proportion of moderate and advanced Parkinson’s patients are severely dyskinetic?

[Andre Turenne:]

Yes. So that’s a hard number to get the precise. But in our experience and working with our investigators, we think it’s a small portion, it’s a minority of patients with severe dyskinesia to the level that we – that would be excluded from this trial. So it’s small percent.

[Jeff Hung:]

So just, I want to make sure that – so then do you think that the three out of 10 excluded from the Phase 1b is representative of what you might see in the real world?

[Andre Turenne:]

No. So there were two reasons why the 10 patients that were in cohorts 2 and 3, likely may not be patients that would be enrolled in the Phase 2. One of the criteria was too severe of dyskinesia. But the other criteria, that’s not more stringent is the amount of OFF time at baseline, which is the disease severity of baseline. So we had a patient population here that we had – it will be more stringent than Phase 2 as stood at the minimum amount of minimum OFF time at baseline. So it's – these two factors that they are enriched if you well into Phase 2 versus Phase 1b experience.

[Jeff Hung:]

All right, great. Thanks for taking the question.

[Operator:]

Thank you. And your next question comes from Jim Birchenough of Wells Fargo. Your line is now open. Again, Jim Birchenough your line is now open. Please check your mute button. And our next question comes from Sumant Kulkarni of Canaccord. Your line is now open.

[Sumant Kulkarni:]

Hi. Thanks for taking my questions. The first one is on the ADC product. At the time, you are eventually in a position to receive Phase 3 data. You'd have a wealth of time build up on the patients that are in the Phase 1, which might inform whether this product is truly a one-time dose or not. So assuming that for some reason ADC does not turn out to be a one-time dose, how many years of an effect do you think it needs to have to compete credibly with deep brain stimulation?

[Andre Turenne:]

Yes. So thanks for the question. So as you say, durability is an important feature of the program an appealing feature. So the evidence that we have – if you go back to the development of the program there, we have up to 15 years of preclinical model in monkeys that show that the durable sustain expression of ADC following treatment with VY-AADC. So that is one signed up. If you administer variety seemed to putamen, which does not degenerate in Parkinson, you have this potential for a very long duration. From the first clinical experience, with the VY-AADC, there is no data to five years prior to the Phase 1b that we've conducted that shows again, durable expression of ADC, and as you suggest, we have a Phase 1b that was a three-year consent and that will also look to have patients in an extension study to be able to continue to collect the data to be able to assess certain the durability of effect in this latest active group of patients. So all of this that definitely will be a part of the full picture by the time we get to BLA filing for the durability of effect. So anything from that experience that suggests multiple years of a durable improvement will be certainly a big, big improvement for these patients. Or otherwise, they really have plateaued and has peak and continue to increase their levodopa dose, while they continue to lose a motor function. So here it's not – what we're seeing today is not just the stabilization of disease, what the data suggests is an improvement in motor function with less background therapy. And if that can be sustained, this is a very important to clinical benefit that we believe.

[Sumant Kulkarni:]

And then given the wrinkle thrown in by the FDA addendum now, I know you said that you're going to announce when you will dose the first patient. How does the timeline on that change though, if, if at all?

[Andre Turenne:]

The plan for such trail does not change. So again, this is the first placebo-controlled study that we're doing with VY-AADC, we think it's in the right patient population and the plan has been reviewed and discussed that with the agency. So I think the question here is the likelihood of the suitability of a single trial as currently size to be sufficient for a BLA filing and that's going to be the core of the question to continue to discuss with the agency. So we can again consider making any adjustments to our plans if and as necessary once we get the greater clarity. With the plan for the current study is as previously planned.

[Sumant Kulkarni:]

Thank you.

[Operator:]

Thank you. And our next question comes from Jim Vrachnas, Wells Fargo. Your line is now open.

[Yanan Zhu:]

Hi. This is Yanan dialing for Jim. Thank you for the questions. So just want to ask about the FDA’s language under the bit more because of the Phase 2 is indeed a randomized design, I think – I think the design was pretty similar to the Phase3. And also given that you already have Phase 1b data, so it's a little curious about the language of a Phase 2 being exploratory. So I guess – what is your thought on that? And then secondarily a given that the Phase 2, Phase 3 are similarly designed. The current designs a staggered starts, but do you have the ability given that your comfort level now it's all the data, do you have the ability to move the famous restart time ahead so that you can still have the similar kind of a timeline for data. Yes. I guess, I'll stop there and have a follow up next.

[Andre Turenne:]

Yes, thank you, Yan for your question. So we'll have to discuss with the agency again to clarify their statements and their position and we'll do as we've done today that we'll look to incorporate that feedback into to inform any adjustments to our plan. So this is a new information to us and we have an ability again to have the next set of discussion with the agency to try to their position and there for us then in turn to make any adjustments as we think helpful and necessary. And again, soon in front of us here before the end of the year, we have a scheduled a Type B meeting and again we have the benefit once again have this RMAT designation that’s the express purpose of this designation is to be able to have the right to access an accelerated type of feedback with the new agency and we’re going to absolutely look to both via the Type B meeting and via the cannel to get the clarity very quickly and then consider any change, if any to deal over all that plan to a BLA.

[Yanan Zhu:]

Got it. Thank you. And also on the posterior study, are we going to have some detailed data on the six months – at the six month follow-up time point or is it just the 12 months, in next year that’s the first time we will hear detail data. And also, have you shared the posterior study data with FDA yet? Thank you.

[Andre Turenne:]

Yes. Thanks for your question there. So, we currently expect to share once we have the full cohort of eight patients, those with the posterior route get to 12 months, which is in Q2, 2019. We’ll expect to provide that full update at that time. And to your other question, the data is going to be submitted to the agency once we have a request for an additional meeting. We’re going to provide the relevant data set to put it in front of them, whether it’s from a updated longer-term results of the 1101 study or results from this 1102 with the posterior route, we will provide the freshest cuts of data relevant for discussions with the agencies moving forward.

[Yanan Zhu:]

Got it, got it. Last question on the preclinical program in Huntington’s. Just wondering, is there a role for coverage, in this disease as it is for Parkinson’s, and in the coverage by the gene therapy of the putamen and now you also mentioned thalamus is also going to be a targeted site, and if there is such a rolling for coverage than what a kind of a percentage of coverage should we expect to be therapeutically relevant? Thank you.

[Andre Turenne:]

Yes. Thanks for the questions. I’ll ask Dinah to answer your question here.

[Dinah Sah:]

Yes, it’s a good question. There is a role for coverage of both the putamen and the thalamus in Huntington’s disease, in the case of the putamen and of course, it’s involved in motor function, the medium spiny neurons throughout the putamen are degenerating, those the ones we want to protect by lowering Huntington. So the broader, the coverage, the more medium spiny neurons we protected, the more benefit to therapeutic benefit to function. With the thalamus, we’re leveraging the widespread and relative and preserved connections to the cortex, and different regions, different nuclei of the thalamus project to different regions of the cortex. So in order to maximize the distribution of our veterans of the cortex, and maximize knockdown of Huntington throughout the cortex, likewise the goal would be to maximize the distribution and coverage of the thalamus. So in both cases, for both structures of the goal would be to cover a large portion of both structures.

[Yanan Zhu:]

Got it. Thank you very much.

[Operator:]

Thank you. And that concludes our question-and-answer session for today. I’d like to turn the conference back over to Andre Turenne for closing remarks.

[Andre Turenne:]

Thank you, operator. So that concludes the call. Thank you all for attending. I appreciate all the thoughtful questions and we’ll look forward to being you on the progress in the near future. Thank you.

[Operator:]

Ladies and gentlemen, thank you for participating in today’s conference. This does conclude the program. You may all disconnect. Everyone. Have a great day.