Editas Medicine Inc (EDIT) Q4 2018 Earnings Conference Call Transcript

Editas Medicine Inc (EDIT -1.92%)
Q4 2018 Earnings Conference Call
Feb. 28, 2019, 5:00 p.m. ET

Contents:

• Prepared Remarks
• Questions and Answers
• Call Participants
  
  

  See all our earnings call transcripts.

Prepared Remarks:

Operator

Good afternoon, and welcome to Editas Medicine's Fourth Quarter and Full Year 2018 Conference Call. All participants are now in listen-only mode. There will be a question-and-answer session at the end of this call. Please be advised that this call is being recorded at the company's request.

I would now like to turn the call over to Mark Mullikin, Senior Director of Finance and Investor Relations at Editas Medicine. Sir?

Mark Mullikin -- Senior Director of Finance and Investor Relations

Thank you, operator. Good afternoon, everyone, and welcome to our four quarter and full year 2018 conference call. Shortly after the market closed, we issued a press release providing our financial results and corporate updates for the fourth quarter and full year 2018. A replay of today's call will be available on the Investors & Media section of our website approximately two hours after its completion. After our prepared remarks, we will open the call for Q&A.

As a reminder, various remarks that we make during this 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. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our most recent quarterly report on Form 10-Q, which is on file with the SEC.

In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligation to update or revise any forward-looking statements, even if our views change.

Now, I will turn the call over to our Chief Executive Officer, Cindy Collins.

Cynthia Collins -- Chief Executive Officer

Thanks Mark. Good afternoon, everyone, and thank you for joining us for our corporate update call for the fourth quarter and full year 2018. In addition to Mark, I'm joined today by several members of our executive team, including Charlie Albright, our Chief Scientific Officer; Vic Myer, our Chief Technology Officer; Andrew Hack, our Chief Financial Officer; and Tim Hunt, our Senior Vice President of Corporate Affairs.

We are at an exciting juncture at Editas Medicine as we enter the clinic with the first in vivo CRISPR medicine to be approved for human testing anywhere in the world, and we wouldn't be here today without our dedicated team of editors who are working to translate the promise of CRISPR gene editing into durable medicines that transform patients' lives.

On today's call, we will review some of what we achieved over the past year and then look ahead to 2019 and beyond. Let's start with just a few of our teams many accomplishments in 2018. We received permission from the FDA to begin clinical trials with our lead experimental medicine EDIT-101 for LCA10, which we expect to be the first in vivo CRISPR medicine administered to patients in history. We advanced our potentially best-in-class CRISPR medicine for sickle cell disease and beta thalassemia, culminating in an oral presentation at the American Society of Hematology in December that was awarded best of ASH by the organizers.

We fortified our intellectual property with favorable court rulings and additional patent issuances and filings. We strengthened the organization with key additions to senior leadership and our board of directors. We expanded and deepened our alliances Allergan and Celgene. Finally, we maintained our strong capital base, providing a robust runway to create transformative medicines four patients and value for shareholders and employees. These accomplishments give us momentum into 2019 when we plan to initiate patient screening mid-year for the Phase 1/2 trial of EDIT-101 and to begin dosing patients in the second half in collaboration with our partner, Allergan.

We expect to begin IND-enabling activities for sickle cell disease and Usher syndrome 2A. We plan to hire outstanding executive leadership to lead our next phase of growth. Lastly, we expect to establish additional strategic alliances to expand and accelerate our development of transformative genomic medicines. This positions us to achieve our EM22 goals for the year 2022 to have at least three experimental medicines in early stage clinical trials, at least in or ready for late-stage clinical trials, and all of this built on a best-in-class pipeline, platform, and culture.

Now, let me turn the call over to our Chief Scientific Officer Charlie Albright to discuss our pipeline progress in more detail.

Charles Albright -- Chief Scientific Officer

Thanks Cindy. I'm excited to be with all of you here today to update you on our progress in both our in vivo CRISPR medicines as well as our engineered cell medicine programs. Starting with the ocular portfolio, we're developing our lead experimental medicine, EDIT-101, for Leber congenital amaurosis type 10 in partnership with Allergan. We were gratified that the FDA accepted the IND for EDIT-101 upon initial review in November. This is even more notable because, as Cindy mentioned, EDIT-101 is poised to be the first in vivo CRISPR medicine administered to patients anywhere in the world. Much of the preclinical work for EDIT-101 in a manuscript that was recently published in Nature Medicine. The acceptance of the IND and manuscript are tangible examples of the quality of the science we are doing here at Editas.

We plan to start screening patients for the Phase 1/2 interventional studies in the middle of the year followed by dosing in the second half. We expect to enroll 10-20 adult and pediatric patients in this open-label dose-escalation study to evaluate the safety and efficacy of EDIT-101. We will test up to three dose levels across five cohorts. We'll start with a low but potentially efficacious dose in adults with more severe vision loss. We will then progress to higher doses in adults with a broader range of vision. Following review of safety data by an independent data monitoring committee, pediatric patients with a range of vision will be included.

As we look forward to dosing patients, it's worth recalling that our preclinical studies in mice and non-human primates showed a rapid onset of editing within a few months following dosing. Productive editing is expected to trigger increased CEP290 protein and thereby growth of the outer segments in the photoreceptors. New outer segments should lead to an ability to sense light and hopefully rescue vision in these patients.

As we advance the interventional study for EDIT-101, we are also conducting a natural history study. The natural history study can enable the interventional study in several key ways. Particularly, the natural history study lets us examine potential endpoints, identify patients, and engage sites. For instance, we have seven sites in the study recruiting across the United States and Europe. We anticipate that these sites will be part of the Phase 1/2 study and longer-term development of the clinical program. We also expect participant demographic and baseline data collected to date to be presented at the Retinal Cell and Gene Therapy Innovation Summit in April.

Beyond EDIT-101, our next program addresses another inherited retinal disease called Usher syndrome type 2A or USH2A. Like LCA10, USH2A effects the photoreceptors. For these reasons, we can leverage almost the entire product construct from EDIT-101, namely the same AAV vector, the same staph aureus Cas9, and the same photoreceptor-specific promoter. We expect that the only difference between EDIT-101 and USH2A therapy will be the guide RNAs, and we believe the similarities de-risk and accelerate our development of the experimental medicine for USH2A. We presented initial data with academic collaborators from Massachusetts Eye and Ear last year and plan to present additional results at the American Society of Gene and Cell Therapy in May.

Finally, it's worth mentioning that our success with staph aureus Cas9 uniquely positions us to develop gene-editing medicines with AAV because strep pyogenes Cas9 is too large to enable the single AAV approach we use with EDIT-101. In addition to the good progress we're making in our ocular pipeline to help patients with serious eye diseases, the learnings from our ocular work position us to begin work in other therapeutic areas where in vivo editing could lead to transformational therapies.

Turning next to our programs in engineered cell medicines, the convergence of gene editing and cell medicine is expanding the kinds of transformative medicines that are now possible. We're working in a number of different cell types for several serious diseases. Let's start with our program to develop a best-in-class engineer cell medicine to treat sickle-cell beta thalassemia. In our approach, we edit sites within the globin locus that increase fetal hemoglobin directly. At the American Society of Hematology meeting, we showed that cells edited at the globin locus repopulated all lineages of the blood system, including importantly the red blood cell precursors.

In contrast, others are editing an enhancer element of the Bcl11A gene that indirectly increases fetal hemoglobin. We found that cells edited at the Bcl11A enhancer had reduced levels of red blood cell precursors and lower editing in those precursor cells had survived. If these preclinical results translate to humans, our editing approach for hemoglobinopathies may yield a medicine that's both safer and more effective than other gene edited medicines in development. Our presentation at ASH was selected as one of 11 best of ASH abstracts chosen from a field of over 5,000, again exemplifying the quality of the science at Editas. Later this year, we will present additional data on this exciting program and initiate IND-enabling activities.

Switching gears to our work in oncology, we're investigating significantly to develop engineered cell medicines to treat cancer. We are advancing programs to address liquid and solid tumors using both autologous and allogeneic approaches. We have programs with Celgene on engineered T-cells and wholly owned programs utilizing natural killer cells. More to come about these programs later in the year

Now I'll turn the call over to our Chief Finance Officer Andrew Hack to discuss how we are building the business and to review our financial results.

Andrew Hack -- Chief Financial Officer

Thanks Charlie. It's my pleasure to update you on key developments in the business and to summarize the financial results we reported today. We made strong progress in building a sustainable and valued business over the past year. In 2018, as part of our strategic collaboration with Allergan, we each exercised our respective options to form a 50/50 co-development and profit sharing partnership for EDIT-101 in the United States. As a result of that decision and the subsequent acceptance of our IND for EDIT-101, we received aggregate milestone payments of $40 million from Allergan.

Outside the US, Allergan remains responsible for both the development and commercialization of EDIT-101 and we are entitled to milestones and a high single-digit royalty on net product sales in those territories. Allergan continues to be an excellent partner and we look forward to executing our US development strategy for EDIT-101 with them in the years ahead. 2018 was also a year of continued success in expanding and fortifying our robust intellectual property portfolio. We were pleased that the US Court of Appeals for the Federal Circuit affirmed the US patent and trademark offices decision that ended the interference concerning foundational patents exclusively licensed to Editas. We believe this ruling invalidates our strategic investment in intellectual property, which includes over 70 issued patents and over 600 pending application for CRISPR/Cas9 in CRISPR/Cpf1, and continues to expand on a regular basis.

Turning to the numbers, we have summarized our financial results for the fourth quarter and full year 2018 in the press release that we made available an hour ago and we expect a file our 10-K shortly. Our cash, cash equivalents, and marketable securities increased $40 million in 2018 to $369 million as of December 31st, 2018 from $329 million as of December 31st, 2017. Our uses of cash totaled $103 million and include cash operating expenses of $98 million and capital expenditures of $5 million. Key non-cash items recording in our income statement include $27 million of stock-based compensation, $14 million of non-cash R&D charges associated with payments to our licensors, and the acquisition of assets from i2 pharmaceuticals, $3 million of depreciation, and a $3 million increase in working capital.

Over the course of the year, we grew the size of our organization by approximately 20%, increasing to 132 full-time employees from 112 at the end of 2017. The primary drivers of growth in our spending in 2018 were our expanding and maturing pipeline and advances in our platform, and we expect these to continue to be the primary drivers of spending growth in 2019. Our sources of cash in 2018 totaled $143 million and consisted of $77 million of equity capital raised, $50 million of milestone payments from our business development partners, $11 million of stock purchased by our employees through stock option exercises and our employee stock purchase plan, and $5 million from various other sources. We believe our year-end cash position of $369 million provides at least 24 months of capital to fund the advancement of multiple transformative experimental medicines.

With that, I hand it back to Cindy.

Cynthia Collins -- Chief Executive Officer

Thanks, Andrew. Before we wrap up our prepared comments, let me briefly remark on our organization's transition to the next phase of growth. We have continued to strengthen the board of directors with my appointment and the addition of Dr. David Scadden announced just weeks ago, and as you know, we are also in the midst of changes to our executive team. I would like to thank our departing CEO, Katrine Bosley and CFO Andrew Hack for their leadership in building Editas, and advancing us toward the clinic with our first experimental medicine. We have active searches for both positions under way with the assistance of leading executive search firms and look forward to appointing outstanding new leaders, as we become a clinical-stage company. We have an exciting year ahead of us as we enter the clinic with our first experimental medicine that we expect to demonstrate the promise and potential of CRISPR technology to transform patients' lives. We expect this to be the first of many as we advance our pipeline in 2019 and beyond. We thank all of you for your interest and support.

With that, we will open up the call for Q&A. Operator?

Questions and Answers:

Operator

Thank you. Ladies and gentlemen, if you have a question at this time, please press the * and then the number 1 key on your touchtone telephone. If your question has been answered or you wish to remove yourself from the queue, please press the # key. Again, that's * then 1 to ask a question. To prevent any background noise, we ask that you please place your line on mute once your question has been stated. Our first question comes from Matthew Edison with Morgan Stanley. Your line is open.

Hannah -- Morgan Stanley -- Analyst

Hi, this is Hannah on for Matthew. I was just wondering, at what stage are your allogeneic programs at, and what are some key differentiating features in your approach versus other CRISPR companies? Thanks.

Vic Myer -- Chief Technology Officer

This is Vic Myer, the chief technology officer. We did recently disclose high-efficiency multi-gene editing and some strategies to ameliorate translocations at the recent Keystone genome engineering meeting. We haven't disclosed the specific nature of the programs or indications that we're going after at this point.

Hannah -- Morgan Stanley -- Analyst

Okay, thank you.

Operator

Our next question comes from Cory Kasimov with JP Morgan. Your line is open.

Matthew -- JP Morgan -- Analyst

Hey guys, thanks for taking my question. This is Matthew on for Cory Just curious, on the heels of your Gamida collaboration and interest in natural killer cells, I'm curious to get your high-level thoughts on how you see autologous CARII approaches fitting into your overall strategy on oncology going forward.

Charles Albright -- Chief Scientific Officer

We really can't comment too much on the autologous too much. That's really a part of our collaboration as you appreciate with Celgene, and we're excited about the tremendous progress we've made there. We achieved four technical milestones there. What I can say is we are excited about natural killer cells. We think they're a different kind of cell that has tremendous potential to be effective in oncology and you'll hear much more about our efforts in that area as the year goes on.

Mathew -- JPMorgan -- Analyst

Okay great, and then on your beta globin program, what are your thoughts on potential differentiators when compared to gene therapy in both beta cell and sickle cell disease?

Charles Albright -- Chief Scientific Officer

Obviously, there are different approaches, and there really isn't a head-to-head comparison in the approaches at this point. I think that gene editing has some significant advantages and that we're recreating what human genetics had led us to, which is to make mutations in the beta globin locus that increase fetal hemoglobin. In that sense, I think we're trying to recapitulate where human genetics has led, and I think that's an interesting way to go.

Mathew -- JPMorgan -- Analyst

Great, thanks for taking my question.

Operator

The next question comes from Whitney Ijem with Guggenheim. Your line is open.

Whitney Ijem -- Guggenheim -- Analyst

Hi guys, thanks for taking the question. Sorry if I missed this, but just wanted to circle back to USH2A. Can you talk about the synergies there between the programs, between that and LCA 10? I'm just wondering if there's any ability to leverage some of the preclinical package to advance into the clinic more rapidly.

Charles Albright -- Chief Science Officer

There are tremendous synergies. This is Charlie. There are tremendous synergies between those two programs, and so the therapeutic approach is quite similar, that we're gonna deliver the gene editing machinery within a single adeno-associated virus, and because we're delivering to photoreceptors in both programs, we'll be able to use the same promoter, the same AAV 5 serotype. Everything will be the same except for the guide RNAs, and so the basis we've constructed in the pharmacology models and how we construct a safety package and our experience with the FDA, we all expect to be able to leverage in the USH2A program Exactly how that plays out and the details of the timeline, we don't really know, but we clearly have done the USH2A program much more rapidly in the discovery phase than it would have without the LCA10 program.

Whitney Ijem -- Guggenheim -- Analyst

Great, thanks.

Operator

Our next question comes from Philip Nadeau with Cowen & Company. Your line is open.

Phil Nadeau -- Cowen & Company -- Analyst

Good afternoon, thanks for taking my questions. First, on the initiation of a clinical trial, can you talk in a little bit more detail about what has to happen between now and when the first patients are screened? Is the bottleneck manufacturing? Is it opening in clinical trial sites? What re the work streams that will take several months?

Charles Albright -- Chief Scientific Officer

We're doing all the things you just mentioned and more. We got the IND approved. We need to get IRB approval and institutional bias safety board approval. We have to get the patients screened and we then eventually have to get them scheduled with what's a surgical procedure on top of delivering the drug, obviously, to the site. I think you can appreciate in these rare diseases that you just can't turn on the spigot in the same way you would in a more common disease or in a trial where you're enrolling healthy volunteers. It's really all the things that go up to the ability to actually dose a patient.

Phil Nadeau -- Cowen & Company -- Analyst

Do you have the drug manufacturer or the therapy manufactured in order to dose the full trial or is there still a manufacturing run that must happen?

Mark Mullikin -- Senior Director of Finance and Investor Relations

Yeah, as I'm sure you're aware, in order to get the IND approved, we've had to have several development runs as well as GMP compatible runs, so we're comfortable with our process and we're comfortable with our network.

Phil Nadeau -- Cowen & Company -- Analyst

Got it, OK. Second, on the Celgene collaboration, obviously they may or may not be subject to a takeout. Is there any change of control provision in that collaboration or does your collaboration go unmodified even if Celgene's part of a bigger organization?

Andrew Hack -- Chief Financial Officer

Hey Phil, it's Andrew. No, there's no change of control that changes the nature of the agreement. If Celgene is acquired or if Celgene is not acquired, the collaboration will continue as planned.

Phil Nadeau -- Cowen & Company -- Analyst

Got it. Andrew, congrats on your tenure Editas. One other financial question for you. On the milestones in the Allergan transaction, can you remind us how they're both -- are they amortized over the life of the agreement?

Andrew Hack -- Chief Financial Officer

Yeah, the $25 million IND acceptance milestone is treated differently than the $15 million milestone associated with the opt-in, and so, we can take it through the accounting in some more detail, but the 25 actually gets treated as contingent consideration and is added to the pool of deferred revenue that gets brought in over time.

Phil Nadeau -- Cowen & Company -- Analyst

Got it, OK, and then one last question for me that's on the patent landscape. First is on the University of California patent that was just issued, what are your perspectives on that patent, and second, are there any patent developments that we should look forward to over the next couple months or quarters?

Andrew Hack -- Chief Financial Officer

Yeah, I'll take that one as well, Phil. Thanks, and thanks for the congratulations. The patent that was recently allowed is one of the patents that was involved in the interference. We expected it to be allowed with the interference having cleared. I think this is obviously a topic that requires a much more detailed discussion, but I feel really good about our IP. This issuance doesn't affect any of our IP, which we think covers all medicines used in CRISPR technology, and I think it's also worth just noting that the way this patent is issuing and some others from U of C are structured. They have key constraints on the guide RNA structure that's covered under that patent, and I think it's worth just reading those claims in some detail to understand those constraints better.

Phil Nadeau -- Cowen & Company -- Analyst

Got it, that's very helpful. Thanks again for taking my questions and congrats on your transition.

Andrew Hack -- Chief Financial Officer

Thanks Phil.

Operator

Our next question comes from Amanda Murphy from BTIG. Your line is open.

Amanda Murphy -- BTIG -- Analyst

Hi, thanks for taking the questions. Good afternoon. I just actually had a follow up on Celgene. I think you've presented some data in the past around key cell editing using Cpf1. Is that part of the Celgene agreement, correct? Then, also, I'm just curious, I know they probably have a lot going on, but have you had any discussions at this point about kind of extending the agreement beyond, I think, 2020, so anything in terms of extending beyond that, have you had those discussions yet?

Vic Myer -- Chief Technology Officer

This is Vic. I'll take the question. Yeah, we've shown highly efficient editing in T-cells with Cpf1, multiple genes, and in fact for all the sort of most likely genes for an allogeneic package. We've shown multiplexing of Cpf1 in primary T-cells as well and we've shown that combining Cas9 and Cpf1 actually reduces the frequency of observed translocations. I can't comment on the nature of the discussions around prolonging the relationship with Celgene.

Amanda Murphy -- BTIG -- Analyst

Okay, got it, and then just on Cpf1, it seems like there are patents being issued everyday on new enzymes, new CRISPR enzymes. I'm just curious if you're seeing anything else that's out there that's interesting that has clinical advantages that you might want to bring in house, whether it be smaller enzymes or easier delivery, packaging into delivery systems.

Vic Myer -- Chief Technology Officer

Yeah, we, of course, keep an eye on the literature, and there's a lot of people working on creating or discovering new molecules. We're really happy with both Cpf1 and Cas9, all the versions of Cas9 that we use. They're complementary in many ways. We can package them up in an AAV, and so we feel really good about those. I think the bar for a new enzyme would have to be very high. We're at 95% or better editing with our two different platforms.

Amanda Murphy -- BTIG -- Analyst

Okay, and then just a last one, kind of continuing that theme. Given you have Cpf1, I mean, obviously you're maybe one of the only CRISPR companies to be able to use a single AAV in terms of delivery, and then obviously you put a lot of work into your guide RNA structure and you might have a little bit of a unique technique or strategy there, as well. I'm just curious if you're seeing interest from pharmaceutical partners in terms of maybe moving into other indications based on those two factors I mentioned.

Vic Myer -- Chief Technology Officer

Yeah, this is Vic again. I mean, we spent a lot of time talking to a lot of people and there's a lot of focus on the field. It's probably inappropriate for me to disclose whom we're speaking with, but I think one of the things we have shown and will continue to show is some of the great advantages that Cpf1 has and how it differentiates itself from Cas9, and there's certainly folks interested in those molecules.

Amanda Murphy -- BTIG -- Analyst

Got it, thanks very much.

Operator

Our next question comes from Gena Wang with Barclays. Your line is open.

Peter -- Barclays -- Analyst

Hi, this is Peter for Gena. Thanks for taking the questions. In terms of EDIT-101 could you give us some color in terms of what happens after doing in terms of timeline? How long is a waiting period between patients within a cohort and between the cohorts, if any? Will there be a DSM-III release between cohorts and/or between patients? I have a follow up.

Charles Albright -- Chief Scientific Officer

Multiple questions imbedded in there, most of which we haven't disclosed. Suffice it to say that the Phase 1/2 trial will be very similar to other gene therapy trials, and there will be a delay between patients and a small delay between cohorts. At times, there will be an independent safety data monitoring review, but that will not happen between every cohort and it'll primarily happen when we head into pediatric patients, but the rest of the timing, you would not be surprised by from what's happened in gene therapy trials.

Peter -- Barclays -- Analyst

Got it, that's helpful. Just in terms of management, organizational changes, would you be able to give us any color on what type of changes to future strategic decisions we could expect, any discussions there, or any visibility into when new leaderships might be in place? Thank you.

Cynthia Collins -- Chief Executive Officer

Sure, this is Cindy, and we have no change in our strategic direction at all. We are focused on EM22, as I stated in my earlier comments, and continue to focus on that as our overall guiding strategy for the company. In terms of recruitment of other C-level positions such as CEO, CFO, again, as I mentioned, we have searches under way. I'm not going to comment on timing because it's just too uncertain, but we feel very good about those searches. The company is in an incredibly strong position. We have outstanding science and a leadership team and getting ready to go into the first clinic, lots of cash in the bank, so all really strong things that candidates would be considering as they think about joining Editas.

Peter -- Barclays -- Analyst

Great, thank you very much.

Operator

Thank you, and as a reminder, ladies and gentlemen, that's * then 1 to ask a question. The next question comes from Peter Lawson with SunTrust Robinson. Your line is open.

Peter Lawson -- SunTrust Robinson -- Analyst

Thanks for taking my questions. I guess, as we think about the natural history study, Charlie, is that still a first-half event?

Charlie Albright -- Chief Science Officer

We will be presenting baseline data in the early part of this year, hopefully at the retinal meeting that we discussed in the prepared remarks. It's important also to realize that the natural history study is not gating in any way for the interventional study. We have a good idea of how to get that going and the natural history study just does other things for us other than start the interventional study.

Peter Lawson -- SunTrust Robinson -- Analyst

Got you, thank you. Then, what could we see in that study? How will the data be presented?

Charlie Albright -- Chief Science Officer

We're looking at the state of a couple things. What are the potential end point we might use in the interventional study? It does several other things for us. It gets the sites up and going, which should dramatically improve the speed of the interventional study and it also begins to identify potential patients for the interventional study, and those are both really important events as you can appreciate, recruiting in these rare diseases is one of the challenges of making them go as quickly as possible.

Peter Lawson -- SunTrust Robinson -- Analyst

Then, for the data for the 101, could that be a 2019 event or how should we think about when we could see that data and what kind of read outs we should have, and the timing around that?

Charlie Albright -- Chief Science Officer

Yeah, we haven't disclosed that. As you can imagine, we're going to be monitoring the data in real time. We're going to be working with our partner Allergan to decide on the right way to disseminate that data. As you can appreciate, there's always the trade-off between wanting to release every piece of data in real time and the notion of being cautious about how we release the data, so we're confident and we see the interpretation, and so, we'll be balancing those competing interests as we think about how to release the data.

Peter Lawson -- SunTrust Robinson -- Analyst

Then, just finally on the cancer program, could you remind us how long was left on the Juno relationship and any timing you know of around IND studies coming out of that program?

Charlie Albright -- Chief Science Officer

Yeah, the Juno, now Celgene, relationship goes until May 2020 as disclosed in our documents, and as the program has transitioned to Celgene, our ability to disclose details of the timing of the programs has changed pretty dramatically as you can appreciate with a large pharmaceutical partner now, and so, unfortunately, we can't say too much about that.

Peter Lawson -- SunTrust Robinson -- Analyst

Got you, OK. Thanks so much for taking the questions.

Charlie Albright -- Chief Science Officer

Thank you.

Operator

Our next question comes from Steven Seedhouse with Raymond James. Your line is open.

Steven Seedhouse -- Raymond James -- Analyst

Hi, good afternoon. Andrew, best of luck in your new endeavor. I just had a question about the LCA10 preclinical data publication from last month. The highest dose of EDIT-101 in mice in that study does not actually lead to the highest editing rate, so it's a pretty interesting result. It dips below the editing rate of a lower dose. The explanation in that paper was for reasons that are unclear at this time. Obviously, we're not under peer review on this call, so I'm just curious, are there any reasons that you can point to that might be leading to that result?

Andrew Hack -- Chief Financial Officer

No, we don't actually understand the reason for that result and it could be for all kind of different reasons, which is why we didn't speculate in the paper, and it is important to realize that that dose is well beyond the dose we anticipate using in humans.

Steven Seedhouse -- Raymond James -- Analyst

Okay. Does the ratio or proportion of productive edits versus nonproductive change depending on the concentration of Cas9 local to the DNA?

Andrew Hack -- Chief Financial Officer

No, it does not. In fact, the entire editing profile is dose independent.

Steven Seedhouse -- Raymond James -- Analyst

Okay. Do you know if AVV 5 capsids in the eye can aggregate?

Andrew Hack -- Chief Financial Officer

No, we don't know the answer to that. What we know is that, very similar to other AAV programs, you do generate an immunogenic response to the capsid and the capsids are transient because there's no way to re express them once the virus has unloaded, if you will.

Steven Seedhouse -- Raymond James -- Analyst

All right, thank you.

Operator

Thank you and I'm not showing any further questions at this time. I'd now like to turn the call back over to Mrs. Cindy Collins, CEO, for any closing remarks.

Cynthia Collins -- Chief Executive Officer

Great. With that, we thank you all for participating in today's call and for your support as we work to bring transformative new medicines to patients. Have a great evening.

Operator

Ladies and gentlemen, thank you for participating in today's conference. This does conclude today's program. You may all disconnect. Everyone have a wonderful day.

Duration: 36 minutes

Call participants:

Mark Mullikin -- Senior Director of Finance and Investor Relations

Cynthia Collins -- Chief Executive Officer

Charles Albright -- Chief Scientific Officer

Andrew Hack -- Chief Financial Officer

Vic Myer -- Chief Technology Officer

Hannah -- Morgan Stanley -- Analyst

Matthew -- JP Morgan -- Analyst

Whitney Ijem -- Guggenheim -- Analyst

Phil Nadeau -- Cowen & Company -- Analyst

Amanda Murphy -- BTIG -- Analyst

Peter -- Barclays -- Analyst

Peter Lawson -- SunTrust Robinson -- Analyst

Steven Seedhouse -- Raymond James -- Analyst

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