All right. Welcome, everyone, to the Global Healthcare Conference of Learing Partners for 2026. I'm Lillian Asango, and I'm joined today by Josh Mendelbrun, the CEO of CAMFOR. Josh, welcome.

Great. Thank you for having us here.

Well, thanks for coming. Maybe we can just dive right in, and I'm just going to give you some time So you can give us an overview of your technology platform, given how differentiated it is from most of the approaches that we encounter.

Yep, absolutely. So maybe I'll just start with the simple tagline. So we use antisense oligonucleotides to increase gene expression. So you can think about us as the inverse of most of the oligo companies in terms of downregulation. Now, the way that we are able to do this is by targeting a new category of RNAs called regulatory RNAs. These are RNAs that come out of the non-coding genome, specifically enhancers and promoters. And what we've discovered through one of our founders, Rick Young, as well as at Camp4, is that every protein coding gene in the human body relies on its own unique set of regulatory RNAs to control gene expression. And we've effectively put together a platform that first and foremost allows us to catalog all of the regulatory RNAs and the genes that they correspond to in any given cell type. And then we've figured out how to selectively drug a regulatory RNA using a standard chemistry ASO to allow us to increase gene expression. And I'd say one of the unique features that differentiates it from sort of the classic RNAs or steric oligos that target mRNA is that by targeting these regulatory RNAs, we can get a very precise upregulation. Unlike microRNAs or long non-coding RNAs that are pleiotropic, this is very specific to the gene region and very controlled as well. But it has very different types of biology, very different kinetics. So that's a lot of what our platform is doing is basically learning that whole new area of biology using ASO chemistry.

So maybe on the fundamental science side of things, So, obviously, when we think about ASO or SIRNA, we think about gene silencing, and for most indications, the more silencing you have, the more knockdown to knockout you have, the better, right? That's the goal. How should we think about that in terms of overexpression? Is there a sweet spot you're trying to reach depending on the indication, or are you going after indications where the more is the better?

Yeah, no, it's a very good question. So to just answer it right from the get-go, there is a sweet spot, at least for the diseases we're focused on, which are haploinsufficient. So mathematically, you are missing 50% of what you need to otherwise be healthy. The sweet spot then is a two-fold increase. And interestingly, that's exactly where this biology takes you. So what we have found, and we've tested this in over 40 different target genes, actually, is that when you do what I just said, so you target a regulatory RNA with an antithythalgonucleotide nucleotide in vivo, you get about a two-fold increase. And interestingly, the cell doesn't want you to go above that. So it governs itself, probably because of toxicity and other cellular mechanisms. So there are hundreds of different haplons efficiencies. Most of them have no approved treatments. And it allows us to basically take the technology there. We get asked from time to time, are you worried about that? That's not something we're concerned with. It tends to hover right around two-fold. So it's sort of the perfect, it's the ideal target space for us to be able to use that technology. You know, interestingly, the one thing that I think is unique about the upregulation field is, you alluded to this, is when you're downregulating things, you're used to seeing curves where you're showing a 90, 95 percent decrease. And it's very clear to see upregulation is a very different field. And when you're dealing with changes that are anywhere from 1.5 to twofold, which is 100 percent, but effectively you have to be able to see the signal through the noise. So we've had many different assays that we've developed in ways of effectively being able to look at the biology and say, okay, that's real. That's an actual increase versus something that's noise. And I think that's one of the sort of most important parts of this new field is that you're just dealing with a whole new way of looking at the biology.

So half low is sufficient indication. You were able to double the expression or bring it to a level that's closer to what you would see in the wild tap. Now, with the approach, how should we think about durability when we compare it to, say, you know, traditional ASOs and RNAIs?

Yeah, I mean, you know, interestingly, so to start with, we're using the same state-of-the-art chemistry that's in approved drugs like Spinraza for SMA. So we're, you know, part of our strategy is to buy down as much risk as we can and not take on things where we, you know, we can't solve that risk. So using chemistries that are known to us, well understood is one area where we do that. It turns out, and by doing that obviously you can look at decades of research and clinical studies and compare and contrast, but the short answer is the pharmacokinetics and the pharmacodynamics. So when we look at the pharmacokinetics specifically, it tends to overlay pretty nicely on what you see actually for other ASOs. And so what that ultimately means is that we think the dosing should be similar to what you'd for your standard ASO chemistry. So that's the good news, is that you get the advantage that we all like with oligos and sRNA, which is sort of longer-lasting dosing.

Great. So now that we've had an overview of the platform, so diving into the program, so obviously you have shifted, you know, from the ureacycle disorder program to prioritizing the SYNGAP program. Before we dive into the SYNGAP program, I wanted to ask if you could walk us through the rationale of the reprioritization, and then any learnings from the UCD program that applies to your understanding of your own platform and as well as, you know, read-throughs to the Syngap program?

As I was walking over here with my CFO, I was like, how do I tell people that I like one child more than the other? And I do it politely. You know, a couple of things. One is, I think, so we are a platform company, but actually what I like to tell people is we are a product company with a platform. And in order to get to that point in time, you really need to, I think, find religion with where your technology works best and also make sure that fits within what the company is capable of doing. So, you know, last year was a year where many companies had to do a lot of thoughtful reprioritization given budget constraints, high cost of capital, et cetera. And we're no different than that. And so that's one feature of it. But the other is that actually just the Syngap program in and of itself, the preclinical data gives us high conviction that it should be successful in the clinic and we can talk more about that. It is a massive unmet need. There's no approved treatments there. And it's a relatively large rare disease. And so we looked at that and we said, okay, this is a very compelling opportunity for CAMP4. Behind that there are other, and we'll talk about this, I know, Syngap-like opportunities. And so we looked at that and we said, okay, this is something where it can be, for example, to use an analogy, RTTR program that we can build from, but in the CNS, right? We saw that we can build an entire pipeline there. Our urea cycle program is a very clever approach. It's also very high unmet need. It is a smaller market, but still a market nonetheless. And it's not a hapline sufficiency, right? So I told you before, we've found that our technology is really well suited for hapline sufficiencies. But I think more importantly, in the liver, we didn't necessarily see a franchise beyond UCD for us to build a pipeline from at Camp 4. And so it was on its own. And so from that perspective, we can only take on so many programs, and we decided for those reasons to shift to Syngap. Now, what we learned from the urea cycle program is a few really important pieces of information. The first is the pharmacokinetics. So we know that targeting now reg RNAs, it seems to be similar to other oligos in terms of what you'd expect. It was very safe, so we had no safety issues whatsoever. And then lastly, as a small company, it was our first time going into the clinic. And I'd say we executed to perfection. Everything was done on time. We did it ex-US in Australia. We just opened a CTA in Europe for that program as well. And so that actually has a lot of read-through to other programs coming down the pipeline, in particular for working with regulatory agencies and how we progress, for example, the SYNGAP program.

So last question on the uricycle disorder program. So as you mentioned, it was a well-designed, and well-executed program clinically. How are the potential partnership discussions evolving?

Yeah, so we just kicked those off in the beginning of the year and just getting going. What I'd say is that there's definitely people, I think, very interested in the program itself. They're following along with it. I think it's more of just a question of finding the right home for somebody who has a franchise that fits in those rare diseases and urea cycle. And so we're in those discussions now and we're hoping that we can give that a home that somebody else can progress it forward.

So now shifting to the favorite child, the SYNGEP program. So can you provide us an overview of the indication and the current management?

Yeah, absolutely. So I mentioned this before. So SYNGEP is a bona fide haploinsufficient disease. So effectively, one of your alleles no longer makes a healthy protein, and that means you essentially make 50% of what you otherwise need to be healthy. These patients have no disease-modifying therapies available to them. In fact, they have almost no therapies available to them. And so, and they range from, it obviously affects children, but these children become adults and then they get institutionalized, so it's a lifelong disease. And the hallmarks of the disease are, first and foremost, you have a learning disability, cognitive impairment, seizures. These kids can have 10, 20 seizures a day. They can't sleep. They have mobility issues. In fact, if you were to go to any of the Cure Syngap Foundation events where many, many families come in, what you'd find is all of the parents have the tattoo, which is essentially bite marks up and down their arms because these kids can't communicate well. And so they're so frustrated with their situation. So it is a really terrible, terrible disease. But really importantly, it is not a neurodegenerative disease. It is a neuroarrest disease, meaning that we think these kids are just stuck in their bodies and that effectively if you can go to the underlying cause of the disease that you should be able to actually ameliorate these symptoms and actually help them live a much better life.

So you mentioned something very important. So you think those patients are kind of stuck and there's a need for like an unlocking that could potentially lead to great improvements. So that's a very selfish question because I've been doing a lot of kind of research on SynGAP and it seems like there hasn't been a consensus in terms of the window of time within which you can have the most impact with a therapy what is your opinion of that and do you think we've reached kind of an understanding of how far can you go before you have done something irreversible or before plasticity is just set and you can't really yeah improve over i don't think i don't think we're anywhere near understanding whether or not and when to your point and i think until we have a therapeutic to test, we won't really know the answer.

Also, I think you hit it on the head, the research, like if, interestingly, the people first say, well, how come I haven't heard of this, right? But then you get very intrigued by the biology. And actually, if you look at the publications from when the gene was discovered in 2009 to, I mean, you have hundreds of publications now about this. So it's very well studied to your point. Interestingly, a couple of things I'll point out. One is at least preclinically. So for example, in our own data, we showed that we could reverse the symptoms of the disease in terms of anxiety and other sort of related phenotypes in a humanized mouse model. Others have done work in older mice and shown that they can reverse the disease as well. So I think preclinically, everybody's done as much as they can do, given the models available to show reversibility. And so that's one piece. Interestingly, I was talking to the head of the foundation and he was saying, you know, as kids progress to adults and get older in life, they actually continue to develop new symptoms, which at at least in his mind, says this disease doesn't just stabilize, it just keeps getting worse and other new things come about. And so even if you're older, you can't necessarily reverse some things. There are still other things that I think actually are really important and can actually keep people from being institutionalized or other issues that are a high cost in the families and the patients themselves. So I think there's a lot of hope to believe that at different stages of life, actually, if you have a therapeutic that deals with the underlying cause of the disease, that you should be able to have a meaningful impact with all that said like any other rare devastating disease the trick is to get in there as early as possible before any damage is done and that's our intention as well so what does that mean as early as possible when we think about potential clinical development right what would be your targets or your ideal target population in terms of age range yeah characteristics as well well so at present and this is a good thing it It used to be very different, but what ends up happening, and let me start with diagnosis because that's actually important. So typically what happens is these children miss a development milestone, a neurodevelopment milestone, and as a parent you can figure that out, or they have seizures. It used to be a diagnostic odyssey, but now with whole genome screenome, whole exome screenome, and genetic panels that have Syngap on it, you immediately get that genetic diagnosis. But that's still about age two or three. So for practical purposes, that's kind of as early as you're going to go. I think that'll change and is changing over time for a lot of different reasons, but our intention is to get down to treat, at least in our first clinical study, as young as two or three years old, let's say. And so those are the conversations we're having with regulatory agencies. And that's really the target population to start with is sort of the, let's say two to 18, but to get as young as possible in that case.

And so one thing that you mentioned is the presentation can vary. It could be seizures, it could be missing some of the milestones. Do you see that heterogeneity as potentially delineating a smaller population that you might target first, or do you intend on just taking any type of clinical presentation?

Yeah, so just to give context to that, so I think about this disease in sort of three buckets. So 80% of patients have truncating mutations, which means they are extremely homogeneous. Those patients, 97% of them tend to have a very high seizure rate, for example. They tend to be very sick. They can't speak, et cetera. There's another 15 to 18% that have missense mutations that are also very, very sick, a little more heterogeneous. And actually, you have 1 to 2% of patients that have a milder mutation that give about 75% levels of Syngap. And actually, you know that they can speak, they can go to special schools, they can respond a little bit to some medicine. So that also tells us that there's a threshold where you get to where you can start to shift this population. So that's useful for us. We're going to start in that 80 percent population. And as you pointed out, we'll try and go as young as possible. And we will set certain thresholds for seizures and whatnot to try and get it as homogeneous as possible. But that'll still, I think, give way to the at least to start with 80% of the population. So we're starting there.

Okay. So we touched upon the target population for clinical development. So as we think about the clinical program, so usually in clinical development, we get sad and then we get mad. But you had mentioned intention of getting mad right away so can you that sounds funny no no sadness just to the madness right away so you know can you kind of walk us through the rationale from for going directly in multiple ascending doze and also what the regulatory feedback has been for that yeah so a couple things um we've benchmarked a lot and recently so meaning looking at all the other companies that have come before us using CNS approaches using oligos.

And it turns out that actually this is not a novel concept, that there are multiple examples of companies that are going right into a mad study. And what's the reason for that? Well, if you have a disease with an extremely high unmet need and you have a product profile that I think the regulatory agencies are comfortable with, and by the way, they're getting more and more and more comfortable with oligos in the CNS because you know, seven, eight years ago, maybe a little longer, we started with Spinraza, right? But now you've had so many things come through that I actually think, you know, we've been very reassured. We haven't talked too publicly about this, but we are having many different conversations with regulatory agencies. And I have to say, it's very reassuring that actually they've come and said, we're comfortable with this. We've seen that. We know this. Like, they're actually telling us what they know. So I think what it comes down to is ethical, where they're like, okay, if I'm just paraphrasing now but if you have something that can help a very sick population we want to make sure we can get you as close as possible to the therapeutic dose to start with and time is your enemy right and so we want to make sure giving a single dose of an intrathecally delivered delivered oligo that's not really going to help anybody a single dose is not some could consider that unethical and I do think that regulatory agencies acknowledge that yeah so I think that's what's behind it. It's more of a balance between what matters more, safety or sort of doing an invasive procedure, if you will, that may not help somebody.

And so you'd mentioned that you've been benchmarking a lot. So with that in mind, can you give us an overview of what is available in terms of natural history and how could that be used during clinical development?

Yep. So even though this disease is a recent one, if you will. And I should say, you know, for those out there, every three to five years, a rare disease gets discovered that nobody's ever heard of, and then becomes the next CF, SMA, et cetera. So I think this is that. And I think the Cure SYNGAP Foundation deserves a lot of credit. They are operating in a very sophisticated and smart way. You need that in these types of diseases. And as a result of that, they're not only preclinical models, but they've actually invested in natural history studies. And there's one in Europe, there's one in the U.S. There's actually quite a few happening. Collectively, there's about 1,300 patient years, which is pretty good. The majority of it is in the younger patients, which is fine, not the older. We'd want to get there. And we've been actually working with them to add additional endpoints for them to be studying as well. So what I can tell you right now is it's a robust data set, and it's helping to inform the design of our phase one, two. I don't think it's quite at the point where you could use it as a control, but that's okay. That's like where we come in and we're starting to collaborate with them and set that up so that it's actually the right data set so that it becomes a tool for regulatory agencies and what it matures at the same time.

Absolutely.

But I've got to say, you know, Penn and CHOP are doing a terrific job. And again, the data they have so far has actually already helped us in thinking about our inclusion exclusion criteria. Back to the question you've asked, which is what's the right population to study this in? So we have really good data there.

So maybe going a little further ahead, how should we think about, well, one, endpoints that matter for that patient population, and two, potential pivotal endpoints?

Yep, so two really important things we think a lot about, which is like we want to show our drug works, we want to show it's safe, and we want to make sure we find the right optimal biological dose. We also want to get this thing to market as quickly as possible for clear reasons. Because we are the first ones bringing a drug into the clinic for Syngap that is disease modifying, we have a real opportunity, but we're also blazing a path. So we don't have anything to compare against yet, right? So we're studying many, many things, ranging from seizures, which many people know is a provable endpoint, and we're going to use video EEGs and home EEGs to sleep scores, to Vineland, to Bailey, because as I mentioned, they have mobility issues and other neurocognitive issues. And, you know, we can look to other diseases as surrogates here. We can look at what they've done, companies have done with Rett syndrome. We can look at what's been done with Dravet, and we can pull that in as well. So that's all been very, very useful for us, and essentially our plan is to bring that all into the study, if you will, and use that to collect many different types of data. Look, we are trying to set up the study to be the most robust way of doing it in the sense that if we have the type of result that gets us those three success criteria, that we can have the write discussions with regulatory agencies about how quickly can we move forward and what does that look like. Whether that's accelerated versus a traditional registrational study, we're trying to be very thoughtful and that includes thinking about a control as well.

So maybe can you give us an overview of the key preclinical data that you have so far that are kind of influencing how you think about clinical development?

Yeah, so So what I can say is from cells in a dish, including patient-derived iPSC cells from SYNGAP patients, all the way through humanized mice that represent the disease to primates, using our human development candidate, we have shown that it can increase mRNA, increase protein, as well as reverse symptoms of the disease. So in the patient-derived cells, we showed we could restore it back to the healthy state. In the humanized mice, I'd say there's two really important things that we showed. And I say humanized because we actually took the regulatory regions that have the RNAs from the human brain into the mice. So it allowed us to use our human candidate. One is it showed us that we could reverse symptoms across multiple metrics of the disease. And I believe we were the first and only ones to do that, which was very, very exciting, if you will. And then I think the other part of it is it allowed us to then go into primates, where that's the clinical route of administration. and what i can say is when you're using oligos or siRNAs against monogenic diseases so single gene diseases and you show a pharmacodynamic marker in primates that tends to translate well into the clinic so that's no guarantee of success but that gives us a ton of confidence both in terms of showing that we could increase twofold that's what we also showed in the mice that when we looked at the protein it was a twofold increase which is a subtle but important point so in haplois efficient states when we use our technology we tend to get about a twofold increase in a wild-type state, like the primates, we get about a 1.5 to 1.7. And again, that goes back to your question of, are you going to overexpress? We think the system doesn't want overexpression, but the fact that we could increase about 50 to 75 percent of normal healthy primates, I think was very impressive, and there were no side effects on those primates either. But we believe in a hapilo-insufficient state, we should be able to restore back to twofold.

So thinking about the learnings from preclinical and then the translation into the clinic, So you had mentioned that in terms of pharmacodynamic, what you've learned so far is that the platform, we can think about it as quite similar to what we've seen with ASOs. How should we think about dosing schedule? And the reason I'm asking is because in the world of ASO and RNAi, what we are seeing is next-generation assets that are leading to more flexibility in dosing schedule, kind of like longer intervals between doses. How should we think about initial dosing schedule as the program moves to the clinic?

Yeah, we think a lot about that, too. I mean, we're already thinking about lifecycle management for the reasons you pointed out. Right now, given the PK characteristics, and we've shown some of this in primates, and we expect it would be similar to what you would have seen in Spinraza or other drugs, which is you do a dose loading maybe once per month for three or four months where you get to a standing concentration of oligos. Oligos tend to have a long half-life, three to six months, and then you spread that dosing every quarterly or every two quarters. Now, we won't know until we get into the clinic and start doing that, But at least the data today suggests that it should be no different than other oligos. So that's our intention as far as we go. You know, in terms of longer lasting, it's interesting. We get asked a lot about shuttle technology, and, you know, that's all interesting. But I'm more intrigued by, for example, what Ionis and Biogen are doing with the Spinarosa 2.0, which is once a year intrathecal, which I think is pretty good. So we're looking at that stuff as well.

I think the patients agree.

Yeah, yeah. I mean, you know, look, intrathecal sounds invasive, but many, many places around the world can do it. It's not something that intimidates them. It's actually they know how to do it. They do it well. And for patients, too, in these diseases, they readily accept it. And so I think the more you can spread it out, actually, the more... Because it gets... By the way, you're putting it directly into the brain. And, like, there's an advantage to that as well. You're not putting it in the rest of the body, too. So there's some advantages.

And so, as we move toward the clinic, can you maybe give us a sense of what are the key remaining steps before the program is in the clinic, it's all set, then, you know, off to pivotal?

Yeah, yeah, yeah. So what we've said publicly, and we've said this at the end of last year, is we have our GLP toxicology studies ongoing. Everybody can do math and knows that should be wrapping up shortly. we're happy with the progress. What else needs to happen? Manufacturing, we're happy with the progress. And then you asked about this earlier, we haven't said publicly, but obviously before you go and you submit CTAs, INDs, et cetera, you have conversations with the regulatory agencies, those have been ongoing as well. So I'd say it's completing our toxicology studies, completing manufacturing, having ongoing discussions with regulatory agencies to basically make sure we're aligned before we submit those applications. And that's all been progressing steadily. Team is heads down. And, you know, we are, I would say, as I alluded to, finding that surprisingly but in a great way, these regulatory agencies are very familiar with these technologies. And it's really reassuring to hear that.

Great. Well, we look forward to the program advancing to the clinic. I also wanted to take a few minutes to talk about the GSK collaboration. Maybe can you give us an overview, but also how should we think about the cadence of potential milestones?

Yeah, so going way back to the beginning, what I just told you was that we use oligos to increase genes. And theoretically, you should be able to do that in any tissue type where you have a specific gene that you want to increase about twofold. And there are both rare and non-rare diseases that fall in that category. Now, we've chosen to build our own pipeline in the CNS, and we can talk a little bit more about what the future looks like there, but there are other tissues where there's lots of good ideas, and we have companies coming to talk to us about that. And so GSK is no different, and they had two large diseases in mind, one in the CNS and one in the kidney, and effectively, they believed they had delivery technology for that kidney as well, and so they came to CAMP4 and said, these are the genes that are underlying these diseases. We're responsible for identifying the regulatory RNA and creating the ASO leads to essentially hand over for them to make products and move forward. So right now, the ball is in our court, so to speak, to do what I just said, which is map out those genes, catalog where the regulatory RNAs are, create the oligos, and then in the future, we get milestones as they start to progress, if you will, those oligos towards the clinic. So it's probably a little too early for us to say that um to give clarity on if you will the milestones but i would say probably not until 2027 is when we'll start seeing more milestones but they give us a very rich up front 17 and a half million to cover that work and so we're quite happy with that okay and how should we think about so you know we've you've mentioned that there are specific type of indications that are great for the platform um how should we think about the partnered indications versus the internal indications?

How would you pick one over the other?

Yeah. So we have this actually worked out and you know that's the advantage of basically behind the scenes doing this over the last seven years. So we're we know essentially. So what simply said there are four or five other ideas we have that are Syngap-like opportunities. What do I mean by that? They're in the brain. They're in the same regions where we know we can get oligo. They have significant unmet needs. There's no approved treatments for them. They're hapal insufficiencies, so they speak to that twofold. And we think we could be the first in the clinic for multiple of them. What I can tell you is we're already working on three DEEs, developmental epileptic encephalopathies. They all fall in that category. We have some early promising data on those. We said publicly we're going to announce at least one of them this year and start letting people know. We're just being quiet about it. So we're holding tightly to those because we think, oh, and by the way, same KOLs, same call points, same academic collaborators. So we see it as a multi-billion dollar franchise. I mean, we think it could be huge for Camp 4, and we think that actually we can own those things. So we're being very selfish about that. We've had multiple companies come talk to us about those, and we've just said we're going to hold on to those right now. So we don't feel the need to own too much else outside of that right now. And so those larger diseases, or I would say things that necessarily you might have a lot of conviction in the gene to increase, but it's not a hapline sufficiency, for example, we're not going to do those right now. And if there's other tissues, we're going to put those in the BD bucket too.

It seems like a very disciplined approach that may lead to kind of like a lot of congruence or overlap between programs so that it's a franchise that's pretty centralized in terms of the expertise that you might need but also the physicians that you might encounter down the road in the commercial space?

Yeah, I mean, I think we have, look, we have a rare opportunity, no pun intended, where if we show, when we show our Syngap program works, first of all, that is a multi-billion dollar opportunity, right? We think it's a big, big opportunity. But because it reads through to the, people ask, does it read through? I'm like, well, it reads through in this case, because the next three to four things after it look and feel just the same way in terms of you're going to look and you're going to say, okay, same brain region, Apple insufficiency, like, if that worked, this should work. So we think it's going to unlock a significant amount of value beyond just the program, but actually into the platform. When do you get platform value as a product company? It's when you can make a plausible claim that things can really read through, and I think this is that. And I think people will see that once we start talking about it more publicly.

Great. Well, we look forward to hearing more about the next program potentially later this year. I'm just going to scan the audience for any questions.

Can you talk about the question?

I want to repeat the question first. Yeah, so the value of targeting regulatory RNA versus mRNA, right. A couple of things. I think traditionally, but I'll say there's caveats to this, targeting mRNA many times was used for down regulation, but there are, of course, examples of where you can do splice switching for upregulation. You know, what I would say we have found as an advantage, aside from just the upregulation writ large, is that it goes back to the basics of the biology, which is every gene relies on these RNAs to control their expression, and these RNAs, these regulatory RNAs are persistent throughout life, so we believe that opens the aperture for a lot more opportunity for upregulation than actually doing splice switching and targeting mRNA. The reason is that every gene makes a different amount of sort of nonproductive mRNA, which is a target for splice switching, and we're just not sure how robust that is in terms of the amount of indications you can go after, whereas in our own hands we think that actually there's quite a lot of different indications you can go after in terms of operating things.

Well, thank you everyone for joining us and thank you for the time.

Thank you so much. Appreciate it.