Editas Medicine, Inc. (EDIT) Earnings Call Transcript & Summary

Good morning from the virtual JPMorgan Healthcare Conference. My name is Cory Kasimov, and it's my pleasure to introduce our next company, Editas Medicine and CEO, Cindy Collins. Please note that following this presentation, we will have a Q&A session where you have the ability to submit questions via the conference portal. So with that, Cindy, thank you for being here today, and let me turn things over to you.

Thank you, Cory, and the JPMorgan team for the opportunity to speak today. Next slide. I would like to draw your attention to the fact that this presentation contains forward-looking statements. We encourage you to review potential risks and uncertainties outlined in our most recent 10-Q and 10-K, which are on file with the SEC. Next slide. Last year was a revolutionary year for gene editing. There were important accomplishments and remarkable strides made towards potentially curative medicines for what were once thought to be untreatable diseases. Gene editing with the help of CRISPR has opened the door of possibilities for patients seeking to cure their genetic diseases. Gene-edited medicines has the potential for superior efficacy, allowing for the treatment of untreatable diseases as well as durable responses, resulting in the promise of onetime curative therapies. They also have the potential for improved safety through greater precision of genomic modifications. Editas is a leader in in vivo and ex vivo gene-editing leveraging our 2 proprietary enzymes, Staph aureus Cas9 and Cas12a. Next slide. Despite the COVID-19 pandemic, we made tremendous progress in 2020. Our lead program is EDIT-101 for LCA10. Last year, we dosed the first patient ever with an in vivo gene-edited medicine. And after completing dosing of the first cohort, are excited to continue the trial. We also regained our ocular programs back from AbbVie and are eager to advance each of these ocular programs now that they are under our full control. We achieved our goal of filing an IND for EDIT-301 for the treatment of sickle cell disease. We also made significant strides in progressing our iPSC-derived NK-cell program for solid tumors. And on the corporate level, we hired 4 highly experienced C-level executives as well as added approximately 50-new editors over the course of the year. We had a favorable patent ruling in the first phase of the ongoing U.S. interference between the Broad Institute and the University of California, with Broad being awarded senior party status in the second phase of the interference. We strengthened our manufacturing capabilities, both internally and externally. And finally, we had a successful capital raise to sustain our operations into 2023. Next slide. All of these efforts continue to strengthen our portfolio. And as you can see, our programs are advancing steadily. Next slide. We plan for 2021 to be another strong year. For our in vivo gene-edited medicines we plan to progress our EDIT-101 brilliance trial and present clinical patient data, most likely at a scientific conference. At the same time, we will continue to further advance our entire ocular portfolio. For our ex vivo gene-edited cell medicines, we plan to initiate the EDIT-301 ruby trial for sickle cell disease as well as file an IND for beta-thalassemia. And in oncology, we plan to advance our ongoing preclinical studies for iPSC-derived NK cells as well as advance the alpha-beta T-cell medicine portfolio with Bristol-Myers Squibb. Next slide. Now turning to our in vivo strategy, where we are the global leader in in-vivo gene editing. Our approach is to develop differentiated gene-edited medicines that can be administered directly to patients. The eye is an excellent starting point for in vivo programs, and we plan to expand our pipeline to several inherited retinal diseases with larger patient populations as we estimate the number of patients affected by inherited retinal diseases to be over 5 million worldwide. In the future, we are also planning to address a wide range of other diseases. The curative potential for gene editing is significant, given that there are over 6,000 genetic disorders. Next slide. One of our primary strategic initiatives is to be a leader in finding cures for inherited retinal diseases, EDIT-101 for LCA10 is our lead program. Patients with LCA10 have a wide range of visual acuity with many essentially born blind. This visual defect is due to a mutation in the gene that encodes the CEP290 protein. Last year, we completed dosing the first cohort of patients and are cleared to move on to the second cohort, the adult mid-dose cohort. Next slide. CEP290 is a protein that is essential for photoreceptor function. Photoreceptors lacking the CEP290 protein have defective outer segments, outer segments are the portion of the photoreceptors that sense light. By correcting the splicing defect in the gene encoding the CEP290 protein, we expect that the photoreceptors will regrow outer segments thereby restoring light sensitivity and hopefully, vision. Next slide. The Brilliance trial for LCA10 is a typical design for this type of rare disease. The primary endpoint is safety. Efficacy is the secondary endpoint, which will be evaluated as we've moved through the different dose cohorts. We started in adult patients with light perception only and with a dose that is on the low end of the range where we expect therapeutic benefit. Our objective is to escalate the dose and eventually move into children with some visual acuity. Based on safety in the first cohort, the protocol has been updated to broaden the inclusion criteria of Sentinel patients, where we will no longer be restricted to light perception only patients. Next slide. As mentioned, we completed dosing of the first cohort last year and after a 9-month evaluation of the first patient and a 3-month evaluation of the second patient there were no reported severe adverse events or dose limited toxicity. We are highly encouraged by this data as it reinforces the safety of our in vivo gene editing approach. We are moving forward to dosing the first patient in the second cohort, which we anticipate will take place in the first quarter. Next slide. Our next most advanced ocular program is EDIT-102 for the treatment of Usher Syndrome 2A. This program benefits tremendously from our work on EDIT-101. EDIT-102 uses much of the same editing machinery as EDIT-101, and we believe this derisk and accelerates our path to decline. We have completed the transfer of manufacturing of EDIT-102 from AbbVie to our CDMO, and we are progressing our USH2A program forward. Next slide. Our third ocular program is aimed at Autosomal Dominant RP4, a progressive cause of blindness due to accumulation of defective rhodopsin protein in photoreceptors. Since RP4 mutations are found throughout the gene, our approach to knock out the endogenous protein and replace it with a wild-type version. We have made excellent progress on this program and plan to identify a development candidate by year-end. Among our strategic initiatives is to become a global leader in finding cures for inherited retinal diseases. These estimated populations reflect the estimated populations with the target mutations of these disorders worldwide. There is a sizable market potential for our 3 leading ocular programs beyond just the developed world. Next slide. Moving on to the second pillar of our strategy, ex vivo gene-edited medicines, where our focus is hemoglobinopathies and oncology. Our differentiated strategy in hemoglobinopathies is to use human genetics to develop a potential best-in-class medicine for sickle cell disease and beta-thalassemia. With EDIT-301, our lead program for sickle cell disease we are able to induce fetal in hemoglobin by editing a site within the beta-globin locus. We are able to edit this site due to our proprietary Cas12a enzyme. And have demonstrated superior preclinical data using this approach. Next slide, sickle cell and beta-thalassemia are diseases of high unmet need. We know from human biology that elevated levels of fetal hemoglobin can dramatically reduce the symptoms of these diseases. We believe EDIT-301 is a best-in-class approach to safely and effectively increase fetal hemoglobin. I am very pleased to say the FDA has cleared the initiation of the EDIT-301 RUBY clinical trial for sickle cell disease, and we plan to file an IND for beta-thalassemia by the end of the year. Next slide. This slide summarizes why we believe EDIT-301 can be best-in-class from both a safety and efficacy perspective. Preclinical data shows that we induce more fetal hemoglobin than the BCL11A enhancer approach. And relative to lentiviral gene therapy, gene editing reduces sickle globin and, therefore, does not have to compete for alpha globin in the same cell. On the safety side, editing at the globin locus, not at the BCL11A locus, stimulates naturally occurring mutations that are found in healthy individuals. Next slide, moving on to the other focus of our gene-edited ex vivo cell medicines, oncology, where we are developing multiplexed gene-edited iPSC-derived NK cells for the treatment of solid tumors. We believe gene-edited NK cell medicines will be the next wave of transformative therapies for cancer patients. Combining the advantages of NK cell therapies with the renewable source of iPSC master cell lines and our proprietary gene-editing technology, we believe we can create best-in-class, off-the-shelf treatments for solid tumor cancers. Next slide. Our iNK program has the benefit of gene editing and cell therapies. We have made substantial progress to date differentiating efficiently edited iPSCs into functional NK cells with potent solid tumor-killing activity. Our iNK program is advancing towards the use of off-the-shelf products, simplifying administration and improving access to treatments to patients. Next slide. We believe gene-edited NK cells will be the future of immuno-oncology. Our approach utilizes the immune system zone mechanism by tapping into numerous advantages of NK cells, which are shown here on the left. We then leverage our proprietary editing technology to further enhance the cells. Our first energy editing strategy is a double knockout of TGF-beta to overcome resistance and tumor suppression and the deletion of cyst to improve persistence and antitumor activity. Next slide. Partnerships have been and will continue to be an important component of building our leadership position. We have been working with Bristol-Myers Squibb to develop the next generation of gene-edited autologous and allogeneic T-cell medicines for cancer. BMS recently declared a development candidate, which resulted in a milestone payment further validating our technology and expertise. We also have 2 important technology-enabling partnerships, our research collaboration with AskBio, is to explore in vivo delivery of gene editing medicines for the treatment of neurological diseases and our BlueRock partnership gives us access to their technology and GMP iPSC cell lines for the enablement of the iNK cell medicines. Next slide. It is truly an extraordinary time to be involved in gene editing medicines. Editas has all the necessary components including an experienced team, development and CMC capabilities, intellectual property and capital to lead in in vivo and ex vivo gene editing. We will have 2 clinical programs in 2021 and will file a third IND for beta-thalassemia by the end of the year. We are committed to bringing transformative, differentiated therapies to patients, which have the potential to be curative and to treat previously untreatable diseases. Thank you.

All right. Terrific. Thank you, Cindy. I will now move on to the Q&A. And again, as a reminder for anyone in the audience who would like to ask a question you're welcome to submit them via the conference portal. We'll get to as many as we can. We have a couple in there already. But Cindy, to start, I just wanted to ask about news you had at the beginning of the week and see if you can provide any color on the departure of your long time Chief Scientific Officer, Charlie Albright, and his reason for leaving and what this means for EDIT going forward?

Of course. And please, Lisa and Michelle, please join me as well. I'm joined today by Dr. Lisa Michaels, our new Chief Medical Officer, who has been with us now about 3 months; and our CFO, Michelle Robertson. So starting with Charlie. Charlie had been with Editas for a little over 4 years and previously had spent the majority of his years at BMS. He is a discovery research scientist by background. And as the company has continued to mature and become more of a clinically focused company, decided that he wanted to return to an earlier stage startup company. So he is leaving, and we'll be joining a new company as CSO. And that company is an early-stage, venture-capital-backed company. We really appreciate all the significant contributions that Charlie made for the company over the past 4 years, building an outstanding scientific organization and advancing the science and certainly wish him well, and we will engage in a search for a replacement for Charlie.

Okay. So that was actually -- it's an understandable reason there. And one of our audience questions is, are you -- do you plan to engage and find a new Chief Scientific Officer. So I guess the answer to that is yes?

Absolutely, yes.

Okay. Perfect. Then moving on to EDIT-101. So you provided some updated time lines, including dosing in additional patient this quarter and potential for data by the end of the year. So maybe this question is for you, Lisa. Why wait until the end of the year, you're starting to have a decent amount of follow-up for the 2 patients you've had in that first cohort where you could potentially see, I guess, some clinical benefit. But when you think big picture, why wait until the end of the year as opposed to providing something on top of just safety right now.

Well, I think at the moment, what I can share very clearly is that the first 2 patients treated who actually are the first 2 patients ever treated with an in vivo editing approach have been able to show both short and midterm safety and that includes follow-up of 3 and 9 months. And I think that's a groundbreaking thing because we didn't see any real problems related to inflammation and that the patients continue to do quite well. As a consequence, it has allowed us to basically increase the inclusion criteria so that we can begin to include patients who don't have limited vision, but in fact, have some ability to have visual acuity that can be purposely measured. And I'm actually very happy that as a consequence of doing that. It reflects the broader patient population and, therefore, has made enrollment much more feasible. So we actually hope to begin treatment in the first cohort just in the next couple of weeks.

Okay. So that makes sense. And then I would assume, one of the things you get by having data later this year is kind of more of a critical mass of robustness for that outcome. But maybe you can help -- it's a little premature given the timing, but perhaps set the bar for that. Some of the key functional secondary endpoints include the mobility core source, a change from baseline in visual acuity, how much of a difference are you looking to see in these types of patients?

Well, I think we have to explore it in a full fashion. The findings from this study will be able to actually inform on the amount of expression -- the amounts of improvement, both in the use of the Mace and also [invesk] visual acuity that we'll be able to obtain. And I think the -- we actually are looking at a wide range of variables that include even anatomical changes, pupilar responses, responses to light as well as visual acuity and the Mace. And I think having a more robust data set will be very helpful for us in terms of being able to define what the endpoints should be as well as setting the bar for how much visual acuity changes we can actually measure.

Okay. And then when you think about recruitment, broadening the inclusion criteria obviously helps quite a bit. You have COVID-19 out there. How much of a headwind is that and can you talk about the interest on the -- within the medical community or kind of engaging in a study like this?

We actually have a fair amount of enthusiasm. With quite a number of investigators who are very interested in participating. I think one of the challenges of the last year has been that the original feasibility assumed that patients would be able or willing to cross different borders and travel across the country, and COVID has certainly put a significant kibosh into that concept and idea. So one of the things that we are actually able to do over the course of the year is identify additional sites and centers as well as follow-up closer to the patients at home. And that is actually helping -- that looks like it will extremely help us in terms of accelerating recruitment.

Okay. And then just last question on this front, going back to safety. I mean, you provided high-level safety update, sounds very encouraging, no serious adverse events or dose-limiting toxicities out as much as 9 months now. Any more granularity you can provide on top of that? Are there -- were there any things that you were looking for in particular that you're happy you didn't see? Or is it just kind of the general nature of how well tolerated it was?

It's sort of the general nature of how they tolerated. Of course, the subretinal injection has associated with its own risks. But additional risks in this particular setting would have been inflammation and whether or not we were able to have controlled immune responses. And I think the most important thing is that the patients were treated with prednisone prophylactically, but there was absolutely no immunologic responses that led us to any concerns about moving on to the next dose cohort.

Okay. And did Spark, in the work they did with LUXTURNA, is that like really helped this process along and kind of pave the way for other companies in terms of treating genetic ocular disorders?

It certainly has provided proof-of-concept of AbbVie on base delivery and also subretinal injection. And I think there's other companies that are sort of following in the same space for other retinal diseases. I think also our nonclinical data was very supportive in terms of being able to define the potential adverse events as well as also the editing efficiency. So I'm very hopeful that the clinical data will continue to support what has been seen in the past.

Okay. And then as long as we're on the ocular front, just one question for me on the EDIT-102 program in Usher Syndrome 2A. As you got rights back to this from AbbVie, have all the CMC activities, things like that been transferred back? Are there any kind of general timelines at least you could provide around this program?

Sure. Well, first of all, we were just thrilled to be able to bring the programs back to Editas, and we were pleased that AbbVie approached us and gave the opportunity for us to do so. All of the programs, as you well know, had originated with Editas, and so we were, I think, the logical home for those. So we have completed all of the transition activities associated with bringing them back those all occurred in the second half of the year, including the transfer of clinical contracts, databases, the IND, et cetera. And then we did wrap up the year in December with a transfer of the CMC activities. So those have been transferred to our CDMO. We haven't given any revised timeline yet on USH2A as we're still digesting the impact of the time line for the USH2A program. We do expect to declare a development candidate for RP4. But one of the advantages with EDIT-102 is it leverages heavily off of EDIT-101 and that a lot of the genetic machinery is the same as EDIT-101. So that should derisk and accelerate that program.

Okay. All right. I want to transition, and I'll follow up with some other ocular questions I've seen from the audience in a moment. But I want to transition to make sure we work in questions on EDIT-301 and now with the IND cleared, do you have a sense of what your initial clinical work is going to look like, what I assume you do, could you share with us? And should we assume that it's going to be along the lines of what bluebird did and what Vertex and CRISPR did with their program in their pilot study.

Well, I think there's a well-paved road to follow here in this particular setting regarding to both this patient selection as well as the process that needs to be put in place to treat the patients. So I think what you're going to see with us is a very similar path in terms of patient enrollment as well as moving forward with treatment. What we're really hoping to be able to differentiate is in terms of the time to engraftment, the levels of hemoglobin F that can be obtained as well as the overall safety of the procedure.

Okay. And so obviously, people will be looking at your program and seeing how that -- those various measures look relative to the ones that are in front the same time, how do you envision staying in front of the next-gen technology. This Is obviously a very hot space right now. So you have the Beam and Graphite and other companies like that, who are moving in here as well. So how do you kind of stay in front and live out your role of kind of being best-in-class?

Well, I think the first thing is we just have to get into the clinic as rapidly and aggressively as possible. And in doing so, we've already identified about 10-sites across the United States that have identified themselves as being very excited to join our study as well as 3 who've already identified patients moving forward. So I'm hoping that as soon as we get the contracts and the protocols through the IRBs that we'll be able to dose a patient once we get into the second half of this year.

Okay. And I was -- my next question was kind of be site interest. And you said it sounds like it's going well, how is it kind of compared relative to your expectations going into this process?

It's actually better than I expected because I was a little bit worried that having a little bit of a later start on this would actually have had some problems with sites. But instead, I've actually been approached by a number of different sites, including places where I have personal relationships where they're encouraged and actually very interested in participating in more than one study.

Okay. And I have an audience question here. What's the differentiation for 301 in terms of sickle cell disease and beta-thalassemia?

So I think the differentiation is really just the targeted mutation. Right now with Vertex, the primary goal has been to turn off BCL11A in our particular setting, what we are doing is we are turning on fetal hemoglobin. and the mutation, which we are inducing a little bit more mimics what's actually seen in, I guess, in the wild, in which hereditary persistence of fetal hemoglobin is associated with a 13-base mutation. That takes place in the beta-globin gene. And that's exactly what we're targeting, so that we're able to effectuate basically a more natural type mutation is not associated with any learn term effects and is known to have long term safety.

Okay. And then this kind of goes across all of your programs, but can you discuss the current manufacturing capabilities at Editas, the capacity from a clinical trial standpoint? And then maybe most importantly, your plans for future in-house manufacturing capabilities. How important is that to you? And how do you think about that investing in that over the kind of near, intermediate and in long term?

Sure. So we have a hybrid approach of manufacturing, and it varies depending on in vivo, ex vivo and the specific programs. And what we've really focused on is really trying to be adaptable and flexible and to go as quickly as we can. So I'll start first with the in vivo gene editing portfolio. Early on, we made the decision to outsource the manufacturing of that pretty much wholeheartedly. So that was an early decision that we made. We decided that we didn't really want to be in the vector production business, and we didn't want to vertically integrate. On the ex vivo side, for both the hemoglobinopathies and oncology programs we decided that we wanted to take on the manufacturing of those programs directly in-house. And so as a result, we ended up leasing GMP clean room space at a nearby facility, we staffed that with Editas personnel, and that really allows us to go very quickly. When we get to large scale, we will also work with a global CDMO, who we signed a 5-year agreement with last year. So it will be a little bit of a hybrid on a go-forward basis. But we also do some internal production at our Boulder facility for a guide RNA as well. So we're really trying to select a manufacturing strategy that is going to be best for what we're trying to accomplish. And to use our capital efficiently as well as go as quickly as we can with the various programs.

How much regulatory feedback do you get prior to making kind of the strategic decisions around manufacturing as you go forward?

I think it's been historically less regulatory-driven as much as it's been just an assessment of our overall skills and capabilities and how we want to use our capital.

Okay. All right. And then on to the NK-cell program, you can just kind of give an overview of the data seen to date and how this is a differentiated modality?

Sure. So first and foremost, we really like NK-cells a lot. They have a lot of inherent benefits, and we do believe that iNKs are going to be the future of immuno-oncology. And as a result, we have been investing quite heavily in the iNK program. We brought in technology and know-how and a GMP cell line from BlueRock Therapeutics about 1.5 years ago, and we're really deploying our expertise in gene editing to create the iNKs. We believe that these medicines are going to require a fair amount of editing and NK cells can definitely withstand a lot of multiplex editing to make them a better medicines overall. We are targeting solid tumors as well. At the ASH meeting this past year, we presented data showing our iNKs with 2 knockouts, one with -- one knockout being TGF-beta, the second being CISH. And we showed that the double knockout edited iNK cells had better tumor-killing potential than unedited cells in an ovarian tumor model. So we're very excited. We think our approach is unique. We haven't disclosed all the EDITs that we're intending to deploy going forward nor have we indicated what indications we're going after, but we do believe that Editas is in a very good position to be able to deliver these cell medicines for the future.

Okay. Great. And then we didn't see an update on EDIT-201, the allogeneic NK-cell program. What's the latest there? Are you just going to go ahead with the iPSC-derived NK cells?

We made a strategic decision at the end of the year after seeing all the great data from all the various companies at ASH, both preclinical and clinical and decided that it was best to really marshal all of our resources on iNK. And so as a result, we decided to terminate that program, but we are taking the learnings and insights that we gain from the work that we did over the past year with that program. We also had a pre-IND meeting with the FDA and got some very positive and an important feedback that we'll deploy in the iNK program as well. But it was really to really ensure that the iNK programs stayed on track or hopefully even accelerated a bit.

Okay. And how should we think about the cadence of events for the NK cell program over the course of 2021? What kind of updates can we look towards?

So we're currently working on preclinical activities, and we hope to be able to present more data later this year. At this point in time, we're not giving any guidance on time line.

Okay. And then as long as I'm asking about news flow over the course of '21, going back to the sickle cell program. Is it reasonable to think you'd have a preliminary update as early as ASH in December? Or should we think of it more as a '22 event?

Lisa, you want to take that one.

Lisa is laughing. I can take that.

My first goal is get my first patient dose. So whether or not we're able to get a long enough follow-up for something, I'm really hopeful, but my fingers are crossed.

Okay. We won't hold you to it then. And then I wanted to ask is probably for -- maybe for any of you, but on the business development side of things, when you're looking forward, how are you thinking about that now either in the form of out-licensing programs as you've done in the past and you got back with AbbVie or bringing in additional tools and/or technologies bringing those in-house to kind of help further your overall platform?

Our business development strategy is really very purposeful as you saw from the presentation, we've had a very productive, long-standing relationship with BMS going back to the origins of Juno and that they're our exclusive partner in the alpha-beta T cell space. And also, we've brought in technologies that we felt were important to enable our various programs. We'll continue to look at those, and we'll do those somewhat opportunistically, but with our purpose.

Okay. And then a couple more audience questions I want to get to. So one is among the many genetic diseases, which ones do you consider most or best suited for your editing approach? Pretty broad question but.

Yes. So today it's largely the ocular diseases. And as I said, we are committed to continuing to develop the ocular programs that we have in inherited retinal disorders, we'll be looking at other ocular diseases as well. We like the eye and that it is an immuno privileged site and by treating an eye at a time, you essentially always have a control. And the amount of vector required to deliver in to the eye is fairly small. But we are looking at other therapeutic areas, other tissues, other organs. And I think the real key there for us will be delivery, and can we effectively deliver to treat a particular disease.

Okay. A couple more investor questions to work in. It follows up on Ocular. Besides the sizing of the various ocular medicine opportunities, is there a greater unmet need in either LCA10, USH2A or RP4?

So of those programs, RP4 is the largest market of the 3 of them, but I view them all as meaningful opportunities to pursue.

Okay. And how well identified are these patients? For those 3 indications? Are they well-known or identified better in one than the other?

Well, I think like many rare diseases, there probably are many patients that have not been appropriately diagnosed. And with the access now to more and more genetic panels and to be able to do more conclusive testing and screening of patients, we hope that we'll identify more patients as well. But I do believe they're probably a fair number of patients that are either misdiagnosed or not diagnosed at all.

I assume that's another front, we're having a commercial product like LUXTURNA might help in the future by the time you guys get to the market. Let me work Michelle and before we wrap up here. And I know you guys are well capitalized. When you talk about the cash runway and just your comfort with kind of your -- where you stand now as you look out with all the things you want to invest in?

Sure, sure. So as you know, midyear in 2020, we did a financing, which put us in a really good position to finish out 2020 and kicking off 2021. We've got enough cash to get into 2023. We do like to have 2 years of cash on hand. So right now, this supports all of our current plans. And -- but we're always thinking about financing relative to the current strategy as well as business development opportunities. But going into the new year, we feel really good with our capital position.

Okay. Another investor question just came in. So we'll get this in and then we'll wrap up. Is there any scientific hurdle to apply gene editing in a bigger indication such as hemophilia?

Lisa.

I guess the real problem that we face with hemophilia is just a very large number of albumins, I think, in hemophilia, there's over 2,000 independent genes that are identified specifically or mutations that are identified that lead to it. So basically, what you wind up having to do is a major knock-in, and I think a lot of people are actually looking at the albumin locus for that that's a big challenge because you have to be able to have a delivery system at high enough efficiency and at the moment with the liver, I think that's still an interesting challenge. But I know there are colleagues out there that are working on it.

Okay. And then we did get another one. So every time I say it's the last one, we have another. In the eye, what is the expected pacing and duration of clinical response?

So that's still very much open in the air at the moment. I'm actually expecting that probably the earliest I would expect to see some changes. And I'm pretty much extrapolating this from other programs, would probably be around the 3-month mark. But because of neuroplasticity and in patients who have the most severe defect, it is very possible that the timelines may be longer.

Okay. Terrific. And with that, I think we'll wrap it up. So thank you all very much. Really appreciate your time here today.

Thanks, Cory.

Thank you.

Thank you.