late.
Right. Right. Right. Right. Okay.
Moderator, could we start? Okay. Great. Great. Thanks, everyone, for being here.
My name is Yanan Zhu. I'm one of the biotech analysts here at Wells Fargo. It is my great pleasure to be doing this fireside chat with Steve Haar, CEO of StandAbout Technology. Steve, thank you so much for being here.
Thank you for having me, and I really appreciate Wells Fargo putting this together. And I'm sure you know we'll be making forward looking statements during this time, and people may want to take a look at our disclosures and risk factors in the 10 Q. We spent a lot of time writing them. They're usually worth reading.
Great. Great. So, Steve, perhaps you could start us off by providing an overview of the company and also review the catalysts investors should pay attention to in the next six to twelve months.
Sure. I like the former question. I'll let you guys figure out what the stock catalysts are. I'm pretty thoughtful on how we're building the business and maybe how we think about progress that we're making, and you guys can figure out what will happen to the stock price. A couple of things that I'll just take a step back.
We were founded with the idea that cell and gene therapy would be one of the more important transformations in medicine over the coming decades. And there's nothing we've seen over the last few years, even though it's been a super challenging field, that in any ways wavers in our view that that's going to happen. We went out and created two technologies. One, really trying to, let's just take a step back, almost every disease that you can think of is caused by either missing or dysfunctional cells. And we thought, the key to replacing a cell is to be able to manufacture it at scale so that it will engraft function and persist.
In order to do all of that, the most fundamental part of that is likely, probably overcoming allogeneic rejection. To date, the way people have grappled with that challenge, and by the way, allogeneic rejection, what that means is you put someone else's cell into your body, your body will see it as foreign and reject it. And the way that people have grappled with that today is one of two things. One is profound immunosuppression, which has a lot of side effects and really limits the applicability of these therapies, or autologous cells. Autologous cells are both difficult and expensive to scale, as well as are only so many cells you can actually really do that, make that kind of therapy with.
So the first thing was overcoming rejection. And I'm happy to say, and we'll walk through this, we have done that. You can see that now in all kinds of preclinical models in animals, nonhuman primates, mice, humanized mice. But we've done it across a couple of different settings in humans and published it in places like CELF journals, and very recently the New England Journal of Medicine. The other technology the company was founded around was the ability to deliver payloads in vivo.
And we call that our fusagen technology. And there, our goal is to deliver different payloads, DNA, RNA, protein, in a cell specific way. And again, think it's an area where we've made real progress. I think we've done it. We've shown we can do this in a very effective way in non human primates.
The field has begun to really pick up with a lot of strategic activity, and we need to show that we can do this in humans. That's the next step in doing that. So what that has left us with is really three categories of therapies that we're pushing forward. The first, and I think the one that has the most external excitement, is type one diabetes. Type one diabetes, as you know, mechanistically is a relatively simple disease.
A patient's immune system just attacks and kills all of the patient's pancreatic beta cells. Pancreatic beta cells are the only cell in our body that is able to make insulin. And up until a hundred years ago, actually a hundred and one years ago to be precise, the diagnosis of type one diabetes is a death sentence. And at that time there was the introduction of exogenous insulin shots. And so where we are today is you have a disease that affects over nine million people.
It's growing actually much faster than the population. Estimates are there will be fifteen million people within about fifteen years. If you have the best possible care in the world, which is in The United States today, you probably have about a decade shorter life expectancy. And if you're not really careful, it's probably more like twenty years shorter. And during that time, life is fraught with side effects from too high of blood sugar like amputation, blindness, kidney failure, heart attack, stroke, and many others.
And you also have the problems with too low blood sugars, which are coma and even death. And it's a it's a hourly burden for patients throughout their life. And so it's an area with a lot of unmet needs and one where we think we can make a substantial difference. I'm sure we're gonna talk about that where we are more broadly, but we've shown in humans that we can trans our goal is very simple. We want to give a single treatment that allows a patient to live for life with normal blood sugars, no more insulin, no more monitoring of their blood glucose, and no immunosuppression.
And it will happen. We may not make it happen, but that outcome will happen and all the component parts now, I think with the data we presented in the England Journal of Medicine are there. The second area for the company, as I mentioned, is this in vivo delivery capability. And we'll get into that, but the area where we're applying that first is the generation of in vivo CAR T cells, basically takes the CAR T process, as you know, from the autologous CAR T setting where the cells are taken from a patient and manufactured into CAR T cells, which are then put back into the patient with the goal of either going after certain blood cancers or autoimmune diseases. Our goal is to do this in a single shot into the patient's vein and to make the CAR T cells inside the body, eliminate the need for things like conditioned chemotherapy, which are very challenging for patients, and hopefully see comparable or better efficacy.
And that's true, we've shown this in non human primates, so we'll come to that. The third area is allogeneic CAR T cells. Allogeneic CAR T cells have been in development for over a decade across multiple different companies. And the biggest challenge that people faced was that this this allogeneic rejection. You put someone else's cells in your body over CMS-four and reject them.
And again, we've shown we've overcome that. So we're developing our allogeneic CAR T cells, one for the treatment of different autoimmune diseases, and two for the treatment of certain blood cancers. And optimistic we have something that really does work. I will say it's a more challenging field right now. I kind of look at the world and I see only a handful, maybe two, stand alone CAR T companies broadly that have a positive enterprise value.
And and we don't always get the privilege of doing what we wanna do. We get the privilege of doing what we wanna do that other people will pay for because we are dependent upon either our investors' capital or some type of a partnership. And so we'll have data that will more clearly define where those drugs are soon, and we'll have to see if that is enough to generate a partnership and or external investor excitement. If if if neither one happens, it may be difficult for us to continue to develop them. So I'll pause there for a minute, but that's really what's going on inside the company across three different areas.
You know, in terms of areas that we think a lot about for marking where we are, this I'll start with I think that the diabetes program can be one of the more valuable therapies in development. It's a very large market that is very unsatiated and where I think we'll be able to the drug works as we hope over time, to sell as much of this as we can make. And so I think the most important value inflection points for the company will be progress with that therapy. If you think about the most important value inflection point, it's showing that our vision is true. And what does that mean?
That is a patient with who has controlled blood sugars with no insulin and no immunosuppression. So we've guided to an IND as early as next year. That means we're trying to get it done next year. That's our every expectation. Things don't always go according to expectations, but we'll see.
And it shouldn't be that long afterwards where you begin to see real proof of concept in people. And we can go through other things. But to me, that's the defining moment for the company that we're really working our way towards.
Great. Thanks thanks for that very comprehensive overview. And
Yeah. Hope I didn't put you to sleep.
No. No. No. This is a riveting.
Eight in the morning. Right? They gotta yeah.
Let's do talk about the type one diabetes program and start from the recent data that you put out. Very exciting data showing that this is an investigator sponsored trial of a primary islet cell. But in that setting, in the first patient treated, those cells appear to be in the body functioning for six months as of the last follow-up, which I think is unprecedented in terms of the duration. I was wondering, has there been additional follow-up since that update? How might the data look? And when might we hear about another update?
I'm going just start by putting these data into context. And so I think one of the things that I mentioned earlier was this disease, type one diabetes, is relatively straightforward. The patient has no pancreatic beta cells. Right? And so I'm going go back and forth.
Pancreatic islet is basically beta cells in a support structure. It's alpha beta cells, beta cells, delta cells. And what was discovered about twenty five years ago and published in the Journal of Medicine by James Shapiro, is that cadaveric islets, meaning taking the pancreas from someone who recently died and donates their pancreas and isolating the islets and transplanting that into a patient can lead to normal blood glucose out now, well out over fifteen years or so. The challenge with that has been that one, cadavers aren't a great source. Right?
And so it's neither replicable, right? There's a lot of variability in the donor, nor is it scalable. And the bigger challenge has been that the patient has to have profound immunosuppression, right, like an organ transplant. And there just aren't that many people for whom lifelong immunosuppression is better than lifelong insulin. The second, over the last few years, we've seen several different parties show that you can take pluripotent stem cells, make them into pancreatic islets, and transplant them into patients and see really, again, great outcomes for these patients.
That is a more scalable source. It is a more replicable source, but you still have the challenge of immunosuppression. And again, there just aren't that many people who that's really the right therapy for. And so our goal here was to show that with the genomic modifications that we make to overcome both allogeneic and autoimmune recognition of these cells, we could transplant allogeneic islets and see no evidence of immunosuppression. That was the goal.
Right? And the way we you know, so it's a it's a phase it's a first in human safety study, and so the dose is low. So the goal wasn't to get the patient off of insulin, and the goal was to show that they did that they would that their immune system wouldn't recognize and kill those cells. And I'd say, you know, hands down mission accomplished. The patient's doing well, all of our endpoints are met.
He's making his own insulin now for the first time since really the nineteen eighties, so in forty some years. And there is very clear evidence by something called c peptide, which is a biomarker. So when a beta cell makes insulin, it actually makes something called proinsulin. And as it's excreted from the cell, it's cleaved into insulin and c peptide. The c peptide is a one to one measure of the amount of insulin that the body is making.
So you see is the patient is making his own insulin. They then had a mixed meal tolerance test, which looks to say, hey, do they function? Do you see increased insulin production when a patient eats? And again, we saw that, and you see it worked very well over the course of the study so far, six months. And you can see with imaging.
So first with MRIs over time and then also with a PET scan that specifically looks for pancreatic beta cells that these cells are surviving. And now you can see with the c peptides, they're functioning. And so it's a it was a great, you know, a great proof of concept. And what it means to me is now all the component parts, you know beta cell transplants work, you know you can make them from stem cells, and you now know that you can gene modify them to hide them from the immune system. So all the component parts are there for that functional cure we talked about, and we just need to make that happen.
Right? And so that patient continues to question continues to be followed. I think in the original discussion of this, we'd mentioned that the patient had been treated in early December, and so that means he's now out over nine months. I don't know. But I I know of of no recent data.
But I would tell you is we will update you over time as the patient continues to do well. I think you should assume the patient does very well. The immune system should have already killed these cells if it was going to. So I would view this material if they die, we'll tell you. If they happen to live, we'll leave it to our investigators to present them at scientific forums because I would presume that's a likely outcome for a while.
Got it. Got it. So as you mentioned, this is the first in human study. So you start the investigators studied, started at very low dose. I think that's roughly seven percent of what's needed for insulin independence.
Do you think as the dose gets higher, you will have the same invasion of the immune system kind of effect?
Yes. Yeah. So this actually one of the things that's interesting about the cadaveric islet, the gene modifications we do are on on cells after they've already differentiated. There are many, of them. And so we're we're pretty good at gene editing, but we're not perfect.
And so we actually because we make three gene modifications, we knock out two genes and we knock one in. Actually, in aggregate, that means that under 50% of the cells had all of the edits we want. And so what you see and there are some cells that have none of the edits you want. Right? What you see then is you actually see in the paper, you can see this, a very robust immune response against the cells that are either unedited or partially edited, and that the cells that are fully edited evade immune detection.
So this isn't immunosuppression. This isn't about dose. At this at this dose, you see a very robust immune response. The difference in the stem cell derived product that we're working on is a 100 of the edits will have the gene modification that we're looking for. Because you start with a single cell, right, we've done all the gene edits to, and we grow them up and then we make them into pancreatic islets.
And so actually, I expect that they will do even better because you won't have an immune response, a local immune response to other cells around you. But there's no every reason to believe, every reason to believe that higher dose will translate to a comparable immune evasion with this. It's not a dose effect. You already know that the dose we've had that there's a robust immune response to unedited cells or partially edited cells. Will this will be fine.
And you also know that you can give people things like vaccines with tiny amounts of dose and that you see robust this isn't the immune system isn't kind of dose dependent. Right? And and it's and it's it's threshold dependent, but not dose dependent.
Yeah. Thanks. That's reassuring. I was wondering, there are additional patients, are there additional patients? Absolutely not.
We have no intention doing that. Okay. The the proof of concept has happened. Right? And and just to give you a sense, I mean, I I know that people think sometimes with n of one, you'd like to see more patients.
To your earlier point, this has never happened before. There's never an example of someone having transplanted cells into a normal immune system without immune rejection. And I think the fact that the New England Journal of Medicine not only chose to publish it, but wrote an editorial which came out yesterday, if you look at the print version of the New England Journal of Medicine, tells you how profound the effect is. So the proof of concept is done. So now we need to focus on the real therapeutic.
And the real therapeutic requires a higher dose, and we would want to move forward with something that you could turn not just into a scientific proof of concept, but a scalable therapeutic that we can get to patients, you know, around the world. We're not interested in in making, you know, in in scientific experiments. We're interested in making therapies for people.
Great. So let's do talk about the path to that iPSC product you're going to put into the clinic. So what are the remaining gating items before you can put that into the clinic? And you did say, that at a recent update that, you had some recent FDA, interact meeting, which increased your confidence in, moving forward with, your iPSC product. Can you share any takeaways from that meeting?
Yeah. Let me just take a step back. The drug is called SC451, and it is a gene modified stem cell derived pancreatic islet therapy. And so what that means is that the first and most important step, and maybe the most challenging step for us to date has been you need to start, you need to make a gene modified master cell bank. So you start your product forever, comes from a single cell. Right?
And so the way we this happened is we took a a host of different cell lines and looked over the course course of the last five, six years, we've looked at a 100 plus lines. We really wanted an o negative line because that can go into every patient. If you use an a positive patient as a donor as an example, then only a or a b blood types will be able to get your therapy. So o negative, which means a hundred percent of the population get this. And we we the goal was to make a cell that was genomically stable over time.
So you're gonna when you grow these cells, just like any cell, you you every time a cell divides, it makes a couple of mistakes. Usually a non coding DNA, it doesn't matter. But when you start with a cell, and every dose is a billion cells. Right? So if you wanna treat a thousand people, you're making a trillion cells.
You want to treat a 100,000 people, you're making a 100,000,000,000,000 cells. You're gonna have a lot of genetic mutations that can accumulate. And if you're not really careful, those mutations will show up in DNA repair enzymes because they're gonna allow the cells to grow faster. And as an example, you don't really wanna I think most people know p fifty three as a mutation, for example. You don't wanna transplant a billion cells in a patient with p fifty three mutation.
That's just probably not a good idea. Right? And so we spent a lot of time and more time than we thought it would in making this master cell bank with a stable genome, meaning that we don't see emergence of problematic mutations. And then also it retains pluripotency, meaning it can go and grow into many many different types of cells, including pancreatic islets. It was way more challenging than we thought it would be, but we've now done that.
And what we really spent time with the FDA is aligning around what the criteria would be for releasing and continuing to maintain that master cell bank. So it's a very big step forward. As far as I'm aware, and again, just talking to potential partners in the large pharma world and things, has been a huge challenge for the field. This is not a SANA specific problem. Making it once you start gene editing these these stem cells, you introduce a lot of genomic instability.
And so really figuring out the cell line, the conditions, and and I think it's a little bit of luck because it's just time to make this happen is a big accomplishment and something that likely gives us a multiple year of competitive advantage and something that should derisk the company dramatically for a long period of time. So what's left to get to the IND now that we have that? We to do the GLP tox study. You have to do it with the cell line that you're going to use. That's your product forever.
Right? And and so we need to get alignment around that cell line. We have to finish that out, and we need to do the GMP manufacturing, tech transfer, and run. Right? So we've been making these cells at a research scale for a long or research with research reagents, I should say, for a long time.
And now we've transferred over to GMP reagents, which has a lot to do with just documentation and documentation at your suppliers and things like that, not just documentation in inside the company. So finish that process, get it into a manufacturing facility, make and release the drug. So finish the tox study, release drug, IND filed, hopefully, then we'll begin to treat patients.
Got it.
And I'll get into this a little bit, but manufacturing these stem cell derived products is not simple. And there are several really important elements to this. I kinda always think about manufacturing as purity potency yield. Right? You're looking at all those things.
And uniquely in this space, purity plays an important role in safety. So purity is often in small molecules, you know, you're just trying to make sure you don't have some weird off target reaction or maybe an allergic reaction to an excipient. Here purity comes down to other cells that you might transplant. And other cells you might transplant can cause tumors and things like that, they're continuing to divide. And so ensuring that we have the right purity and potency is really really important.
And we'll get to yield at some point, I'm sure, because scaling these is very complicated.
Got it. Got it. And the FDA interact meeting takeaways, if any?
As I said, I think we have alignment a way to go. Two two things. Alignment in our around the master cell. There's a there's a pre master cell bank, there's a master cell bank, and there's a working cell bank. So pre master cell bank is the cells you actually start with.
You take them, and you make master cell bank. That's your product for forever. Right? And you need many, many vials of that, and then you make a working cell bank that you make the drug from each time. So alignment around what that all looks like.
And then the other is most alignment around most of our our our preclinical testing package from the Interact meeting. These days, most of is there are certain elements that you can't discuss at the Interact that require the pre IND meeting and and so that's that's not what happened. It happened separately.
Got it. And IND could happen as early as 2026.
Yeah. Right? I We always say as early as and and I I it's a it's a convention we adopted a while ago. That means it's our goal, but we also wanna, you know, articulate and make sure you recognize that we don't always some of our goals can get hit. Right?
And, you know, science is complicated and things can have a little bit of a setback. And so but it's our goal. I think we've got a nice buffer built in. It's every expectation we have right now, but we also understand this is really novel science, and it may not happen next year.
Got it. Got it. And maybe two questions on the desired product pro, profile. One on durability. What is the minimum bar, that will be required by patients, physicians for this type of treatment? I I think you
I think the minimum bar required by the patients is likely a lot lower than the minimum bar required by us. I think if you were to ask a patient and they were to get this for example once per year, they'd be very happy with that. I mean if you could imagine all the injections that they deal with on a daily basis. This is a very complex drug to manufacture and scale. And I think if a patient ended up being treated once per year, it wouldn't be commercially viable.
It's just, we wouldn't be able to make enough of it and the cost of goods would be too high. So I don't yet know where that bar really sits from a company perspective. My guess is you want it to last at least five to ten years. And I would love it to last for life. There's not a reason why it shouldn't last for life biologically.
And so that will be our goal is that it lasts a long long time, hopefully many decades. If you just take the scale challenge here, so 15,000,000 people in 02/1940, that means you treat a hundred thousand patients per year, and that's it. No one else ever gets the disease is stable from there. Stops growing. Right?
A hundred thousand people per year, which would be an enormously successful cell therapy and an enormously successful drug, I think. It would take you a hundred and fifty years to treat all the people around the world. If you just did The United States, it would take you over twenty five years. And so that just gives you a sense of the scale challenge ahead of us. So if we are now having to treat every patient every five years or something, that becomes something we're never going to be able to meet our goal, which is to make this drug very broadly accessible to patients around the world.
Got it. That's a very helpful way to look at this topic. On delivery, you know, do you intend it to be a fully insulin independent? And if so, I think you would need to put in 15 times more cells than what the IST, put in. Right?
So So, yeah, so the the field is actually pretty well defined around this. And and I I don't know if these numbers are gonna be exactly where we end up. But, you know, if you look at cadaveric islets, you know, people have been doing them. There are thousands of them have been done. It typically takes two to four different pancreases of the donor pancreas to get that to work.
It's around a billion cells. Right? So Vertex just published their program in the New England Journal of Medicine, and their dose is eight hundred million cells. So just think of it as circa billion cells. I mean, just plus or minus.
And we might be and and the variables in that that have to work through, one, our manufacturing process, we may end up with slightly different potency than some of these. It might be a little higher or might be a little lower. Right? The second is immunosuppression, in particular the calcineurin inhibitors that are used in immunosuppression are actually quite toxic to these drugs, and sorry, this therapy, the beta cells. And so it may be because of that we get away with a lower dose.
And there's some evidence of that from the cadaveric islet field that when you give rid of the calcineurin inhibitors, have a better effect. The third is our site of delivery is different and so the most common way to deliver these cells is through an intraportal injection, meaning into the portal vein, which is a big vein that drains into your liver. And there are a couple of challenges with that, not very scalable, has to be done under interventional radiology. Two, when cells go into your blood, they shouldn't be there. It's usually a tumor or something.
So we have something called an immediate blood mediated immune response, IBMIR, that will kill many cells right away. And hopefully we don't have that. You know, and and and then the cells may just engraft differently in the liver versus where we plan to put them, which is in the muscle. And so that may lead to a higher dose, it may lead to a lower dose. But when you're thinking about what's the dose, just think circa a billion cells.
And it's practical to put that many into the the muscle in the arm. Right? It is practical to put that in. And just again, even as you look at the cell dose that was delivered in the study of the Uppsala study, remember the majority of cells were gene edited. So you were delivering several 100,000,000 cells to get the, you know, let's call it 60 to 80,000,000 cells that were all gene edited.
Right? And so it's very it's very practical, but exactly how we do that and in what muscle or muscles, might wanna do muscles, is something we're still working through. Because you don't wanna do is inject a big bolus of liquid and create like a compartment syndrome inside of your muscle. You need to get perfusion. And you can see, if you look at those if you look at the pictures, the MRIs in the limb of drill medicine, what you'll see is little dots.
Right? And those little dots are little pellets or beads. They're not really beads, but they're little aggregations that are put in there. So you don't want to just object a big old bolus of cells and it's a gradual injection as the needle is being pulled back.
Yeah. Yeah. Great. Thanks for all those insights. Perhaps let's talk about the in vivo CAR T efforts here.
I think this is certainly an area that's getting attention from pharma. Kite did a deal. AstraZeneca did a deal. AbbVie did also earlier did a deal. So, you know, are you getting interest from pharma for your program?
Could this potentially be an area for non dilutive financing through partnership?
Maybe. Let's take a step back. So what we're trying to do is deliver cells, I said deliver genetic material to T cells, right, to make a CAR T cell and hopefully have the therapeutic effect of that CAR T cell that we're intending. And so we started with making a CD 19 CAR T cell, right? So you could do this with other targets, and that drug is called SG299.
In non human primates, we've shown that we can get we have very cell specific delivery. You don't see any signal in the liver, GLP tox study or gonadal tissue or other tissues. Right? And you get a really nice delivery of payload. Right?
And we've shown that we get deep b cell depletion. I mean, you can't find b cells even in lymph nodes. And that when they do come back, you get this b cell reset that people have been looking for in the autoimmune space. So I think that what we've shown in the preclinical setting is a best in class profile, and that that best in class profile is true if you believe that cell specific delivery really matters. So you don't want to have off target cells, and you believe you want to have integrating DNA, right, to really kind of offer expansion with CAR T cells.
And if you think that you can use non specific delivery, others are actually quite good at that. And we just may have made things too complicated. Right? If that's what you believe. But the thing that you've seen in all of the strategic transactions is at least some human data, which we don't have.
Right? And so most likely to really unlock value, human data is is very, very important. And so where are we in that process? You know, we're we're ready to move towards an IND. The long pole in the tent for that is the GMP manufacturing, which is about a let's just call it about a year from when we say go.
And what's preventing us from saying go right now is is is we need we need money to move this forward. This is not an easy time to be doing cell and gene therapy. We think that type one diabetes is a very very unique and high return, risk adjusted return opportunity. And so in order to move through this IND, we need to bring capital into the either in the comp into the company in some way or spin this out to move it forward. And so we will either find the money, may wait a little bit of time till our cost of capital is lower, partner this as you mentioned.
But with a partnership, the most important part of that for me is enabling this to move forward because I think there's a lot of value in our life. And or spin it out into some kind of a, let's call it, a majority owned entity where capital is really dedicated to pushing just that therapy forward. So I think that, to your point, given all of the strategic activity in this space, a little bit of human data can unlock a lot of value with this platform.
Got it.
And it's not gonna work it's not gonna work for just one therapy.
It's one of these things where it either doesn't work, which again, think we've got really promising non human primary data, we need to see that in humans. And if it does work, it's likely going to work for multiple different CARs. It's unlikely to be just one. It's going to be CD19, BCMA, and a whole host of other novel targets.
Right. Right. Lastly, if we may briefly touch on your allogeneic effort, can you talk about where the programs is the differentiation from other allogeneic efforts, other companies?
I think the differentiation of other allogeneic efforts is that we overcome allogeneic rejection. Right? And we're able to do this with we call bone lymphodepletion with autologous CAR T cell. Again, we've shown that. It's now been published.
It was published in a cell journal just last week. Again, looking at the human data from those studies showing that we've overcome the allogeneic recognition and rejection of these cells. So that gives us an opportunity to hopefully move forward with a profile that is comparable, or maybe even better, but hopefully comparable to autologous CAR T cells efficacy both in oncology and autoimmune setting, and with a much easier and more scalable manufacturing process. So that's what's different. That's our goal.
You know, I think we have to show that we can do that in humans, and those are the data that we will have hopefully soon. And then we need to make sure that someone moves this forward. My sense is investors are so skeptical on the CAR T cell space. Again, every most every company has negative enterprise value that, you know, it will be a therapy that will do better. We move forward with a partner.
There's, you know, again, there's the pharmaceutical industry is much more optimistic than investors are around what this can do. And and hopefully we're able to just do something like that. If we can't get a partner for this, it's unlikely to move forward. You know, I think we will be able to do that though.
Got it. With that, I think we are out of time. So I wanted to thank you Steve for your insight and for being with us.
Thanks everybody for their time and attention.
Great. Everyone have a great day.