All right, thanks for joining us, everybody. I'm Terence Flynn, the U.S. biopharm analyst here at Morgan Stanley. Very pleased to be hosting Editas. Today from the company, we have Gilmore O'Neill, who's the company's CEO, and Erick Lucero, who's the company's CFO. Before we get started, for important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. Thank you so much for joining us. I don't know if you guys want to make any prepared remarks, or you want to go right into my questions?
You know, I think go straight into the questions.
Okay.
Just, you know, great to be here. Very excited to be here to talk about what we're doing.
Great.
At Editas, both what we've achieved over the last couple of years and, you know, where we're going over the next, and what we're going to be sharing over the next six months from a catalyst point.
Great. Sounds good, so last year, you know, there was a reprioritization of the pipeline. Maybe just give us a mark to market on kind of where we stand with, you know, that update, and then the overall strategy and direction, for the company.
Absolutely. For just to set it, the refocusing of the company focused on three pillars. The strategy one was to drive reniz-cel, a differentiated autologous edited ex vivo approach to sickle cell disease. We actually also rebuilt our discovery to focus on in vivo, which we believe is really the future of editing, and I can come back to that in a second. The third pillar really was to exploit the IP that we have as an alternative source of non-dilutive financing. You know, we've actually made a lot of progress against all three pillars. On the reniz-cel side, we do have a clearly differentiated profile, an incredibly exciting efficacy. Something I think is worth pausing sometimes, because sometimes we forget.
I certainly forget, because I look at it so often, but in my career in drug development, I've never seen efficacy like that. In the history of therapeutics, we haven't seen efficacy like we've seen with edited, you know, gene-edited products, where essentially we are taking patients, in our case, with multiple severe vaso-occlusive events from their sickle cell disease, and after treatment, they have no vaso-occlusive events. In addition, these patients are profoundly anemic, and after treatment, all the patients have corrected their anemia. They're actually in the normal range of hemoglobin. So this is incredibly potent efficacy. We don't use the word, we're very cautious about using the word curative, but this is essentially we're certainly. That disease process is arrested completely, and their anemia is corrected.
So we've shared data on 18 patients at EHA from an efficacy point of view just three months ago. We announced that we had dosed more than 20 patients. We announced that we had fully enrolled the adult cohort. Since then, we have dosed more patients, and we announced it as our second quarter call that we've completed enrollment of our adolescent cohort, actually ahead of schedule. Again, a reflection, I think, of the enthusiasm and excitement around this therapy. So that's kind of reniz-cel. Then from the point of view of in vivo, we're actually. We've made a lot of progress, you know, both in-house and with external collaborations on delivery, which is a critical element of in vivo editing.
We are focused on a number of tissues to which we want to deliver ex vivo, with one that we've disclosed, which is hematopoietic stem cells, for obvious reasons. It, you know, builds on the promise of reniz-cel, and then actually tissues looking beyond that. I can return to that more, but we've actually a particularly robust philosophy around how we select the diseases that we do, and also how we approach it from an editing point of view. We want to use a very differentiated approach to editing. We're not knocking things down. We are actually focused on functional upregulation. That's a key differentiator in two ways. First, it differentiates from what siRNA and antisense approaches can do, which are largely almost entirely focused on and only able to knock things down.
And then within our space, it's really an area where others really haven't chosen to go so far. So that's really important because it essentially allows us to go to white space. And then finally, from a target selection point of view, we're very much focused on the curative potential of these in vivo therapeutics, where being first to market or best in class is going to be critical. And in that context, we are making a number of important choices. Beyond just functional upregulation, we actually are focusing on diseases where the standard of care is either poor or non-existent, either within the entire population or a refractory subpopulation. That's because we want to be clearly differentiated from a commercial and efficacy point of view.
In addition, we are particularly interested in areas where there are biochemical marks that give you a rapid readout, and then finally, we're very much focused on de-risking from a regulatory benefit-risk point of view to ensure that by focusing on orphan-sized populations, we can make sure the regulators are confident about the benefit-risk and the use of new technology as we go into therapeutic space. However, we also have to balance that very realistically with, you know, the impact on public health, and frankly, the commercial value.
And so in many ways, one ideal sweet spot is to focus on target indications where a subsegment of a population is refractory, and once you've actually developed and optimized or declared your benefit risk, you can actually life cycle into a larger population without necessarily developing new molecules. And of course, finally, the beauty of the technology is that when you have your delivery and your editing tool combined and maximized or optimized for a particular tissue or cell type. The beauty of CRISPR editing is you change 20 nucleotides on the guide, and you've moved to a new target. Now, it's not quite as simple as that. I don't want to disrespect the science.
There's a lot of important elements in collecting, but it's certainly a lot simpler than building a new antibody or building a new small molecule framework, or structure. So overall, that is, you know, really where we are driving for and for in vivo, and I think very importantly, we are on track for that in vivo proof concept by the end of the year. And then finally, on the IP side, from that third pillar of IP and monetization, we did a very nice deal with Vertex. And actually, I'll let Eric, our CFO, tell you more about that.
Well, thanks, Gilmore. Yeah, we're really excited about the opportunity to get non-dilutive financing for the company via the licensing business that we have. We believe the Cas9 patent that we've licensed from Harvard MIT Broad is a foundational necessary for freedom to operate, and there's a lot of companies out there that are in development, and we believe this is something that we should be able to collect a Cabilly-like royalty. If you remember Cabilly, it was a low single-digit antibody royalty that everybody paid back in the day. So we're really excited about this as a way to help fund our business, and we're interested in working with anybody, and we can create sort of a bespoke way to do this based on each company and where they are in development.
Okay, great. I think there are a lot to unpack there. Maybe, you know, the first one I had as a follow-up is just that, you know, you touched on this a little bit, Gilmore, is just the differentiation, so focused on upregulation, not knockdown.
Yeah.
As we think about your platform versus others, is that the key feature, or are there other features that, you know, whether it's delivery or whether it's the, you know, the size of the edit, like, what other distinguishing features do you think?
Yeah
... you're focused on as we think about the forward here?
Well, I think the way to think about it is that ultimately, the products that we will make and the therapies we make for patients really require a combination of technologies, but actually also philosophies, and so if you look at the in vivo, it's about your targeted delivery, it's about the tool that you use to edit, and it's also about your philosophical approach. Do you upregulate or not? Now, obviously, upregulation is something we can actually do with an indel technology, which is what we have not only very robust expertise in, but we've actually clinically validated. We're talking about using a Cas12a enzyme, which we have clinically validated. You know, we have human data for that enzyme in the editing of human genomes in humans, so that's the third part, second part.
The philosophy of upregulation is an area that we've really embraced, and that's because, one, we believe that's a way where you can truly differentiate, and two, because we've actually validated. We've actually shown that you can do that in humans. In reniz-cel, that's exactly what we've done. We've actually created an edit in a sort of repressor or suppressor element of the HBG1, HBG2 promoter. That is the gene or genes that actually generate gamma globin, and by upregulating gamma globin, we're using it as a functional homolog or a compensator for, in the context of sickle cell disease, aberrant or dysfunctional beta globin, or in the context of thalassemia, missing or absent or underexpressed beta globin. That's essentially what you call sort of almost like the validation of this approach.
Yep. What are some other areas in terms of disease areas where that approach, you might be able to take that approach? Or what's that opportunity?
Yeah
... set look like, where both you have an opportunity to do a knock-in, but also you have the ability to deliver the machinery?
Yeah. So, you go back to two elements. One is the ability to deliver-
Yeah
... to that particular cell type. You know, we've articulated interest in a number of of tissues. You know, liver is obviously one that people have shown they can deliver to. The differentiation approach there is by functionally upregulating. You differentiate from people where most other, in fact, almost all other approaches are knocking down in the liver. So that really opens up a whole new white space, and I'll return to that in a second. The other is if you look at somewhere like the hematopoietic stem cell-
Yeah
... which is an area of particular interest for us. So that's the first piece. I think from the point of view of the diseases that you can approach beyond those tissues, you know, obviously, you can target hematologic diseases with HSCs in the context of the liver. You have a broad swathe of diseases that you can approach. More importantly, what do we know genetically? So one of the focuses we have had in the rebuilding of and refocusing our discovery group is actually building and incorporating statistical genetics. The power of human genetics, I think, sometimes is underappreciated, and it's true value from a de-risking point of view and identification point of view.
One of the things that's happened over the last ten years that really enables us to truly use human genomics, has been the explosion of computing capacity, even without including machine learning and AI, just computing capacity. And the second has been the creation of really very large, nicely, really superbly curated genotype, phenotype, biobank datasets, not just, you know, in the United States, but around the world, which enable us to interrogate them, not just for interesting diseases, but very importantly, to interrogate them and identify natural variants that can actually give you essentially an allelic dose response, which substantially de-risks the selection of a target. In other words, put another way, it essentially replicates what we've done or leveraged to select our target for reniz-cel.
That is an example of where we essentially, well, others actually, in decades before, identified a condition called hereditary persistence of fetal hemoglobin. Then about three or actually four decades ago, the mutations or variants, genetic variants that actually caused persistent expression of fetal hemoglobin were identified. And then, at the same time, the coincident inheritance of persistence of fetal hemoglobin with a sickle cell genotype results in a recognition that patients or warriors who had that co-inheritance had either minimal manifestation disease or substantially reduced manifestation disease. That's an example of how a natural variant driving upregulation of a functional homologue led to a therapeutic strategy and massively de-risked it. So I think that's a wonderful case study of what we're actually doing.
And I would say, as we interrogate the data, which is what I'm trying to say is that, very long-windedly, and my apologies, is that there are functional homologues, and frankly, they're also in the context of diseases of haploinsufficiency, where one disease gene copy and another has a normal gene copy. You can actually upregulate the normal copy to compensate for the loss of the disease copy. So there are many examples across a multiplicity of diseases that enable us to actually take a very broad approach. So with the right targeting strategy and with that approach, we can actually zero in on sort of a range of diseases, which gives us the chance to essentially optimize our selection from a public health point of view and really to find that sweet spot that I've outlined before.
Before we get to reniz-cel, when will we know more about that selection process and where you guys are in that kind of choice of next candidate and seeing kind of some of the efforts from the in vivo and the genetic work you guys are doing?
So we haven't specified a forum or a specific date or format for sharing that, but we are on track for human, or not human, sorry, excuse me, in vivo POC by the end of the year. What we would plan to talk about is, you know, the degree of editing we're seeing and probably just to enable modeling, you know, describe without actually explicitly identifying the genetic target, talk about the size, the prevalence of the population, the TAM, the total addressable market, and other critical elements, so people can actually model. Why not share the specifics of the target or the actual genetic target?
Largely because we do want to maintain some competitive advantage, for the time being, and make sure that we have the opportunity to really progress that, to create value for, you know, our patients and, you know, our investors.
Yep. Can you... Is it, is this a primate model? Is it a mouse model? Can you say anything about...
We haven't specified-
Okay.
We haven't specified species-
Okay
... but obviously, we have a number of different,
Yeah
in vivo models at our disposal
Okay
that we're actively using. Yeah.
And is it you can't say anything about the delivery? Is it LNP, or you aren't saying that?
I think we can talk a bit about that. We really have sort of taken a very focused approach to delivery. You know, I think LNPs have really been what I would say is the key lead validated nanoparticle for delivery.
Mm-hmm.
And so that's an area that we actually have doubled down internally and externally.
Okay.
And then in addition, we obviously are looking. We have a weather eye to, you know, future and promising nanoparticle technologies. But that's where we're focused on. We did have AAV, you know, two years ago-
Right
... but we decided that really from a point of view of focus, building that core expertise, we should actually, leave that to the side.
Okay, great. So LNP, and again, it's liver, maybe hematopoietic products, stem cell, those are like the two-
Yeah
potential organs, and then again, animal species, not disclosed. Okay.
Yes.
And then-
But functional upregulation is a very-
Upregulation
Critical distinction. Yeah.
Yep.
We're not knocking things down.
Yeah. Okay. And what would be, like, what would be a typical development timeline then to advance that to an IND filing, like posting this proof of concept at your end?
It's interesting to use the word typical.
Yeah
... considering that the evolution of in vivo editing is really right now, it's happening as we speak.
Right.
You know, I think some of the factors that will impact it, obviously, are the scaling up. You know, at a manufacturing side, I think that's probably the, you know, what probably the critical thing on the critical path, and obviously, that's the kind of thing that we would disclose at an appropriate time when we have those elements that we're working on really nailed down.
So is it, is it again, months or is it years?
As I say, it's not months.
Okay.
It's something that we would actually, I'd say, one of the things, one of the rules that we've adopted here over the last couple of years is that if we actually say we're gonna do something, we have a greater than 85% probability of delivering on that. So when we actually have much more clarity and are ready to share that, we share that-
Okay
at the right time.
Okay, fair enough. So going back to reniz-cel here, kind of the initial proof of concept of the platform. Again, you know, you mentioned the data that we got at EHA. You've now dosed over 20 patients. Again, I think one question out there in the investment community is just differentiation versus Casgevy and Lyfgenia here. And so just remind us, as you think about that target product profile and differentiation.
Mm-hmm
... what are you pointing people to as kind of the key points as we think about, you know, evaluating, reniz-cel versus these, these other products?
From a key point of view, we would point to the absence of the VOEs we've seen to date. But very importantly, and I think it's a critical differentiator, we have seen correction of anemia in all patients. And not just, you know, scraping across the lower limit of normal. All patients with five months or more of follow-up have shown a durable correction of their anemia, which is well within the normal range. I think that's a very important differentiator. You know, when we talk to our hematology colleagues, they say it's kind of a no-brainer that this makes a difference. So the choice is, do you have a patient who has their VOEs controlled but remains anemic, or you have a patient whose VOE is controlled and actually has a normal hemoglobin?
So those are critical elements. I think the other elements that we're actually very pleased with, from a CMC/IP point of view, we are well advanced and have made a significant progress when it comes to success, you know, successful manufacturing. Indeed, that has exceeded our expectations, so we believe that certainly is going to be a very important potential element. When we talk to, you know, prescribers at treatment centers, there are a number of things that they think are important beyond just the efficacy parameters such as anemia, but actually also the support and frankly, the success and confidence in the successful manufacturing are very important elements that they will consider.
Yep. Okay, I'll come back to the CMC side on a follow-up, but the one I just want to get a sense is what, in terms of this year-end update, you know, I'm assuming ASH is the target venue. What? Like, how much data, how much more follow-up? Like, maybe help level set expectations for what we'll get in this year-end update.
Yeah, so we haven't shared the exact forum, obviously abstracts, et cetera, et cetera.
Yeah.
From a point of view of what we're sharing, we will be sharing data both from our RUBY sickle cell study-
Yeah
... as well as from our thalassemia, EdiTHAL study. We presented data at EHA for 25 hematological patients, seven from EdiTHAL, 18 from RUBY. As I said, we'd already, at that time, dosed more than 20 patients. We've continued to dose. And so when we're closer to the, you know, the end of the year, we'll be able to share exact numbers of what we want. But we're certainly in a very good place when you actually compare or look at the benchmark for a BLA that we use from Vertex, who basically filed with 20 patients and then a supplemental 10 patients. So that can. So we're very good about that. And then from the EdiTHAL point of view, we will have more patients to present as well.
More importantly, I would say, as importantly, we will have longer follow-up for our patients, and we anticipate to may continue to see a very durable effect both on fetal hemoglobin expression as well as the maintenance of correction anemia.
Yeah. And Ryan, what month was EHA in June?
EHA was in June.
So you have another six months-
Mm-hmm
... effectively to follow up.
Yeah.
Okay. Okay, got it. Okay, great. And on the follow-up side, I know again, we have the benchmark for Casgevy from the, the BLA filing side. I think they had 16 months of follow-up.
It's 16 to 18 months-
Yeah
... is their minimum follow-up-
So you guys will-
The FFC cohort.
Right. You'll be in a similar benchmark in terms of duration of follow-up when we see this year-end update?
Some patients will certainly-
Yeah
... have more than exceeded that.
Okay.
Some will be at that level, and obviously, we would be very close from a benchmark point of view, the number of patients as well.
Yeah.
And then it is just a matter of-
Following
... you know, following them up.
Okay.
Yeah.
What time point would you have about a similar amount of follow-up?
If the benchmark was 30 patients-
Yeah
... with eighteen months of follow-up-
Yeah
... you know, I think people will be able to infer from-
Okay
... what we present at the end of the year.
Okay, got it. I guess the other, you know, question we get is just commercial strategy here. Just given, you know, Vertex and Bluebird are building the market right now.
Yeah.
I think there's still ongoing work, but, you know, how do you think about kind of navigating that as being kind of the, you know, the third to market here in the space? What are, you know, some things you can leverage, and what are-
Yeah
... gonna be some of the challenges as you think about bringing another product?
Great question. I've done a lot of talking. I'm going to-
Okay.
Let Terry-
Thanks, Gilmore. Yeah. Now, we're really excited to be a fast follower. I mean, I've spent fifteen years on the buy side. This is a classic fast follower business. If you look at some of the things that Vertex and Bluebird are doing, which have taken time, you have to contract with the centers. That has been taking, you know, one to two years, and that time will shrink as the contracts become standardized. You have to get the therapies included in the state Medicaid budgets. That obviously, the first time you go through that, it takes some time. By the time we get to market, that should be a repeat process. There's patient education. They need to learn about the therapy, and so on and so forth.
So all of those things are happening right now, and we're really excited to kinda come in with hopefully a, you know, better product, and we'll see how that goes. You know, we have said many times we're open to OUS partnerships, and those discussions can go lots of different ways. So I'd say in terms of the commercial launch, the most important thing is putting the patients and the shareholders first. We wanna make sure we get the drug to as many people as possible and the best way to generate returns for the shareholders. So I'd say we're evaluating all options with respect to the structure of that launch, but we're really excited to be a fast follower with a differentiated molecule and build that in a capital efficient way.
Yeah. If you don't have a partnership at the time of launch, would you wait on the OUS launch, or, like, would you focus on the U.S., or?
Yeah, you would focus on the US because obviously we need someone to do the-
Yeah
... development and regulatory, to meet the certain requirements of the EMA or wherever else.
Okay. Okay, so there's gonna be-
And indeed-
... additional
There would be additional work. Yeah, I mean, some of that can be leveraged, and Gilmore-
Yeah
... knows more about that than I do.
So I've worked across the spaces. We actually made the determination to focus on the U.S., you know, very soon after I joined at Editas, and you know, that's been our focus. There is no doubt that most of the information we can leverage. There will be some elements that you'd have to create, but for ex-U.S.
Okay.
But, you know, the bottom line is-
Yeah
is that we have focused.
Okay, understood.
- on the United States.
And then obviously, the, you know, the pricing side, there was some differential between these-
Yeah
Two products. Just strategically, how do you think about that in the aspect of, again, being a fast follower and-
Yeah, I mean, I think the ICER guidance was around $2 million. So I think that's a pretty good proxy. Obviously, you have Bluebird at $3 million and Vertex at $2 million. We don't know what the gross to net is, but I don't think there's any reason to really go outside of that range, just given the health economic benefits that we have from sort of third-party people.
Yeah. Okay. And then in terms of like, again, let's assume, you know, US build, what does that, you know, sales force, infrastructure, investment look like as you think about that requirement? 'Cause obviously, that's something you've got to start planning for here if you're getting close to the, the-
Yeah
... BLA filing.
Yeah, that's something we've thought very carefully about. I mean, I think there are a couple of things that we're saying is management at Editas is not filled with a bunch of starry-eyed idealists. You know, I think Eric has said it very well. We're very conscious about getting the optimal balance for getting the medicine to patients, but actually also with the context we're sure. So we're being very careful about how we spend. You know, the interesting thing about this kind of space and this highly specialized space is that the commercial model may not be kind of your typical model, you know, from a sales force planning point of view. So we're very conscious about that. We're thinking very creatively about that. We're learning from the experiences of Vertex and Bluebird.
We're actually, frankly, not only just going to learn from this, we're going to leverage what they're doing, and as I say, keep a very close eye on the optimal way and most creative way to ensure that we get the spend to value balance correct.
Right.
From a market standpoint, I think there's about 75 centers in the U.S. that are 80% of the volume, and I think a lot of those centers are in the states that you would expect them to be in, based on the demographics. So this is not sort of the, you know, Super Bowl advertising-
Mm-hmm
Mass market. It's
It's highly targeted.
It's a highly targeted specialty pharma.
So you're talking about, like, tens of, tens of reps?
It's closer to that than thousands, yes.
Yes.
But we're still working on the details of that.
Okay.
Again, being a faster follower, we can watch all that, and I think we're not only gonna learn from the sales forces that they have, but are there better ways to provide service? There's gonna be a service component to this. These patients have a long journey.
Yeah
and we think that there are ways to differentiate what we do, and we're gonna watch and learn.
Yeah.
It's really TBD.
Right. Okay, maybe one other follow-up is, you know, Gilmore, you mentioned the CMC side, you've been pleased with what you've seen. Does that imply that you think you can have, you know, a shorter than six-month turnaround time? I know that's something that, you know, Casgevy is kind of from what we've heard, it's about a six-month turnaround time.
Yeah.
Is there room to improve upon that?
Actually, we've actually done a lot of optimization turnaround time. I would say the key variables now that drive turnaround times are the yield, you know, from apheresis. Actually, we've actually had very good success when you actually align that to what we need, in the context of Cas12, so we're actually very pleased with that. Another element is of these patients, these warriors, in our trials are actually very ill. You know, these are patients who, on average, have had, prior to treatment, four serious vaso-occlusive events per year, each year for the two years prior. So when you think about that, you know, when you're during apheresis and even during editing, it's likely that they could have another vaso-occlusive event.
Obviously, going through the rigors of transplant, you want patients, these warriors, to be at the, in the optimal state of health, so they need to recover from the vaso-occlusive event. Those are kind of the variables. It's probably more host, dare I say, or the variance around the patient that actually impact. Obviously, they also want to go through fertility preservation, where this new hope presents itself. They have a medicine which suddenly says, "Hang on a second, this could transform my life. Now, I can think about things like having a family." Obviously, maybe something that they had given up on, but suddenly now this hope is there, so that preservation. Those are probably the key drivers.
I would actually say from a CMC, a manufacturing point of view, we've really brought those timelines very tightly down, and that includes also the QC.
Okay
... and QA, elements.
Okay. So, but it's six months. It sounds like there's variability, but you're not confident it's gonna be meaningfully below that at this point, I guess, by reading the time-
No, we can't. I mean, it depends really very much on, basically, I would say it depends very much on the patient.
Yeah.
You know, from a turnaround point of view, at the manufacturing point of view, we have the timelines actually really quite tight.
Okay.
Yeah.
Okay, got it. Okay, I guess the, you know, Eric, you mentioned some of the third pillar, the IP monetization-
Yeah
- strategy, and again, I remember Cabilly. I started off covering PDLI back in the day.
Oh, yeah.
I remember up-
I remember that.
Yep.
Yeah.
And so, know that pretty well. I mean, as you think about, you know, obviously, you have the one license already, but how many-
We have several. Yeah
... potential? So what I'm saying, like, what's the opportunity set out there?
Yeah.
Because, again, like, there was visibility on a lot of companies that were leveraging, you know, the monoclonal antibody technology.
Yeah.
But as we think about, you know, how many companies are out there looking to access this technology?
Right now, we've identified about 100 different programs. Half of those are at 10 companies, which I'm sure you all know the name of who they are. So that's the kind of market that we're talking about here.
Okay, and have you said, like, how many of those companies you've already had discussions with, or can you give any details on that?
Yeah, we haven't disclosed that yet. I mean, all I can say is we're open to discussions. We're very interested in creating a win-win deal for all the companies that are out there. If you look at what we did on one end with Vertex, that was something that was really designed for a large multinational public company on the eve of launch. What we did on the other end of the spectrum with Vor Biopharma, which was an earlier company, not as large as Vertex, less cash, less resources, that we structured something that met the needs of both of those. But as you think about, well, what is the economic value of these? Think about that Cabilly royalty rate.
Think about the consensus revenues that may exist for any product, and then as you probability adjust that for technical success and time value of that in terms of where they are in development. It's very easy to get to kinda what the economic value is from there. And there are no real debate over, you know, the Cabilly rate, sort of is what it is. That's the standard freedom-to-operate license, and everything else is just time value of money. So it's fairly-
Okay.
Fairly easy.
Okay, great. The other thing I want to touch on is you recently announced this, two-year extension to your collaboration with, Bristol Myers.
Yeah.
Maybe just any more details on that, and what are the milestones that we should think about, in terms of that collaboration?
You know, I think there are no real new elements of the extension. It's very similar. Essentially, we just extended what we already have, and it has been a very successful collaboration. You know, just last year, when BMS updated their R&D, they had an R&D day, and now it sits on their R&D web site. They actually shared six targets that you know which actually represent six of thirteen opt-ins that they worked on. And indeed, we've had, out of that collaboration, two DCs, and we have one at least that's in IND enabling talks. So, we're very happy with how that collaboration has worked. I think they're very happy with it.
I think that extension reflects that, and I think it creates opportunity for, you know, both of us to, you know, maximize value. I think it actually also highlights something else that I didn't touch on when I was talking about, you know, our approach to in vivo. We actually have consciously stepped away from oncology, but BMS is a wonderful example of how we can use our technology, enable its use, in the oncology sphere, even if we're not actually focused on that ourselves. And the reason I highlight that is because when we look at in vivo, I have really probably bored you to tears in continuously emphasizing our differentiated approach to upregulation.
However, there are many organizations out there that maybe have franchises that are in particular areas where there is a knockdown strategy being used today, and where they have a desire to protect that franchise or explore or have skin in that game. We are certainly very able to do something along the lines with BMS, where we can create a package and give a license, and you know, some know-how, for building that, maybe a knockdown. But where we're going to direct our capital is on upregulation, but we're actually also going to ensure that we maximize the use of our technology across,
Yeah
... other elements or, how should I say, areas of opportunity for gene editing.
Okay.
and those packages can be developed inexpensively by us and give us a twenty-year composition of matter.
Yeah
... patent, so.
Okay, and is that so? It sounds like... And again, I don't remember if the target was disclosed for the first IND. It has not?
No.
Okay. All right.
And that really sits... You know, BMS will disclose that.
But it sounds like it's oncology and in vivo knockdowns.
Yeah. I mean, I, I think that, and you can see that on there.
Okay.
Yeah.
Yeah.
Yeah.
Okay. Okay, got it.
It's not in vivo, so these are ex vivo.
Oh, this is an ex vivo.
This is ex vivo.
This is ex vivo.
I'm just trying to use an example.
Okay, got it.
Forgive me, I was using that as an example. Forgive me if I caused-
Okay, got it.
... confusion, but as an example of how we can ensure that even in areas where we're not playing ourselves, the technology is there-
Yeah
... for others to use.
Okay. Well, I think we're up against time, but, thank you very much, guys.
Thank you.
Pleasure, and appreciate the comments. Thank you. Thank you again.
Thank you very much.
Great to have you.