Welcome to the Cantor Global Healthcare Conference. I'm Pete Stavropoulos, Biotech Analyst with Cantor. With us, we have Annexon, a company I do cover, and I am pleased to introduce Douglas Love, President and CEO. So, welcome, Doug. You know, could start off with a brief introduction and a description of the company for those not familiar. You know, sort of your key therapeutic strategy, you know, which is a focus on the complement cascade.
Yeah, absolutely. Well, first of all, thank you, Cantor and Pete, for having us here today. We're delighted to be here and share an update on Annexon Biosciences. For those who don't know us, Annexon is focused on complement, and specifically the classical pathway. Our target is C1q, the initiator of the pathway, and it's quite a unique target. So its key differentiator, for those who know complement, from the downstream components, C3 and C5, is that C1q localizes on diseased tissue, anchors the complement system, and drives a deleterious complement inflammation throughout the body, the brain, and the eye. And we're doing just that. We're targeting or blocking C1q in the body, brain, and the eye to stop autoimmune conditions, as well as neurodegenerative conditions of the brain and the eye. So we're really excited about what we've seen thus far.
We've got robust proof of concept in multiple clinical programs, with our most advanced program being Guillain-Barré syndrome, which I'm sure we'll talk about today.
With the phase III data set, geographic atrophy, which is also in a large phase III program, and our first-in-class small molecule, ANX1502, targeting a host of autoimmune conditions with an oral tablet.
Peripheral.
Peripheral.
There you go.
Exactly.
You know, I guess, you know, like you just mentioned, the most advanced program is GBS.
You got phase III pivotal study data readout earlier this year. Just briefly go over the key data points, you know, that demonstrated efficacy, but before that, you know, just go into a little bit of detail of why you chose to collapse the GBS DS into a three-grade scale, rather than keep it the original seven-grade scale.
Yeah. For those who are not familiar, GBS is an acute neuromuscular antibody-mediated disease. It is the number one cause of acute neuromuscular paralysis in the world, and it's really quite a gnarly disease. So the way it works is, a patient will get some type of preceding infection, oftentimes food poisoning or something or another. The complement or immune system will kick on to clear the body of pathogens and viruses by using inflammation through the classical complement pathway. That clears up your food poisoning. However, two or three weeks later, the complement system turns back on, inflammation attacks your peripheral nerves, and it results in, again, very rapid ascending paralysis throughout the body. One in four patients are going on a ventilator. We've been really focused on this disease over the last 10 years.
We're the only company to run three studies in this space, and there have been no placebo-controlled studies run here in almost 40 years, and so a real intentionality about targeting this devastating disease, for which there are no approved therapies in the U.S. The primary endpoint for this disease is the Guillain-Barré Disability Scale. Excuse me. This is a scale that is one to six, a very discrete scale, with one being normal and six being death. In between there, you have different steps of progression of the disease, so five is patients who are on a ventilator, four, patients who are bedbound, three are patients who have inability to walk, two, you can walk without assistance, and one, you can run.
We collapsed the scale into three buckets with in agreement with the FDA to really make it more interpretable for the layperson as well as clinicians in how they use the scale. So we bucketed it into a good state of health, which is zero to one, disability, which is two and three, and severe disability, which is the remainder of the scale. Importantly, to enter into our study, you had to have disability or severe disability, meaning you were a three, inability to walk without assistance or worse, and that's what we studied in the program.
Yeah. You know, just make a comment on GBS. You know, it's supposedly, you know, not very, very common, but I know at least three people have had it, and I remember one of my friends in mid-twenties when he had it, and you know, he got hit hard.
Yeah.
And, he never fully recovered, you know? And so there's definitely-
It's a rare disease, no question, but more common than what people know, and certainly debilitating. What's really devastating about GBS is it can happen to any one of us. It's completely indiscriminate. You're healthy one day, and the next day you are completely bedbound, and it's really devastating, and many people never fully recover. We've heard so many stories. They're heartbreaking, and so we're really playing with our hearts and minds to tackle it, which leads us to our phase III pivotal data. We released the first phase III placebo-controlled data set in this space in over 40 years, this summer in June, and we were really, really quite pleased with the outcomes of the study across all measures of the GBS Disability Scale and other measures.
Importantly, we had statistical significance on the primary endpoint with this, which is GBS disability at week eight, so we showed a more than twofold benefit in taking our drug versus placebo at week eight. But also, we had impact at every time point in this disease. So starting as early as week one, which is the key prognostic measurement for how patients are going to fare with the disease, highly statistically significant, both on muscle strength as well as GBS disability, and every time point thereafter out to week 26. So an early, rapid treatment effect that was quite durable out to six months, really with the aim of trying to help patients get back their lives as quickly as possible. We also showed improvement on things like muscle strength, which is important. You need to be able to pick up your remote, the ability to walk, et cetera.
We had really outsized impact on days on ventilation. So in our study, we were able to get patients off a ventilator a month earlier than the placebo arm, and we were able to get them ability to walk a month sooner than the placebo arm. So getting patients out of the hospital much more rapidly and allowing them to get to more complete recovery.
Yeah, which I think are very important factors and would definitely have a pharmacoeconomic benefit, you know, especially the ventilator, you know, where even several days has an impact.
Right. Absolutely.
So, all right, I guess, you know, one of the questions we heard, you know, when the data came out, and I'm sure you consistently hear, is dose response. So, you know, you lose efficacy at the higher dose. You know, can you just talk about the biological rationale for why a higher dose may not be as efficacious?
Yeah, absolutely. So we had two doses in the study, a 75 mg per kg and a 30 mg per kg. And as Pete alluded to, we saw greater efficacy at the lower dose, 30 mg per kg. But this is a very different treatment paradigm than what you would think in a standard chronic indication. GBS is an acute monophasic disease, which means there is a specific disease window by which you want to block complement activity, and then you want complement activity to come back and be part of the repair or cleanup process. We saw in our early study, the proof of concept study, that the lower dose, both doses fully inhibit complement. So that's the first thing I'll say. The lower dose inhibits complement for about a week, the higher dose for about two to three weeks.
In our proof of concept study, we saw greater efficacy in the lower dose. It was a very small study, so we decided to take two doses into the phase III study. We took alpha, importantly, on both doses. So you really only needed to win on one of the two doses. And what we saw is robust data on the lower dose, which inhibited complement for about a week and then allowed complement to come back to help repair and clean up, and clear up the disease activity. Um, for the higher dose, not as effective, and what we saw there is we inhibited complement into after the disease process, where you needed to clear up or to repair to come in with complement. And so we really narrowed in on the treatment window for targeting GBS. And importantly, this data is consistent with other data sets.
So when you look at IVIG, which is the drug that is used most readily in this disease population, there it's an unapproved therapy, but they've run studies where they've done one course of therapy and two courses of therapy. And with one course of treatment, they had some treatment effect. With two courses of treatment, they really lose their treatment effect, and their safety events began to increase. And so it really does evidence that you want to treat for a minimum period of time, stop the disease process, and then allow the patients to be in a recovery period more readily.
Okay. You know, and I guess another question often asked is whether the neurotype observed in the Bangladeshi in Bangladesh is similar to that of the Western population, you know, namely, AMAN or AIDP. You know, how translatable are the data to the Western population?
Yeah, good question. So there are really, in effect, three neurotypes . I mean, we talk about two, but there's... So there's AMAN, AIDP, and then there's indeterminate-
Yeah
... where patients kind of float back and forth. What we've learned, which has really been well published on by the experts in this space over the last decade, is that neurotype is not really the key prognostic factor for how patients are gonna fare with the disease. The key prognostic factor for this disease is a patient's baseline muscle strength, which accounts for 70%-80% of how the patients are going to do. How severely disabled are you at baseline? How severely disabled are you at week one? And so that is really the key assessment.
When you look at the comparability of the patients in our study with the Western world, we know that more than half of the patients in our study met the criteria for what patients look like in the Western world based on their baseline muscle strength, which is the key prognostic factor. We're really quite encouraged that the data that we've produced in this study is really generalizable to not only the West, but throughout the entire globe, which we're really excited about. There are 150,000 GBS patients worldwide, and we want to treat all of them.
All right. You know, I guess, for a BLA filing, two things are required. You check the box off in terms of the phase III, but you do need something called a real-world evidence study. So can you just describe what this is, and how it's being conducted?
Yeah, absolutely. So as you said, two requirements for an approval with GBS. One is establishing substantial evidence, which we did with our phase III study. The second is really demonstrating that the outcomes with our data are generalizable around the world. And that is because the study was run exclusively in Southeast Asia. It was unethical to run a study in the U.S. and withhold IVIG for patients who are in a neuromuscular emergency. So that was with agreement with the FDA, with the SAP in place in and around that. And so to do that, we are matching patients in our study with patients from the Western world using a 2,000-patient natural history study, the IGOS, or International Guillain-Barré Outcomes Study, Observational Study. This is being run out of Erasmus.
Most all developed countries in the world are participants of it, as well as many developing countries, and so what we're doing is we're matching the patients in our study from Southeast Asia with similarly looking patients in the Western world, predominantly based on their baseline muscle strength and their GBS Disability Scale at baseline, making sure that the disease of GBS is consistent in Southeast Asia with the disease here in the U.S., and that patients fare very similarly. Really, this all comes down to the generalizability of ANX005 to treat GBS wherever you are in the world and see consistent outcomes. We did that with our proof of concept study. That was successful. We submitted that data to get orphan drug designation in Europe, and now we're repeating that exercise with our phase III data, and we're confident that we'll be able to do the same.
Okay, and sort of what is the endpoint that you'll be looking at?
We're looking at a propensity score matching, so we're looking to show how similar the patients are at baseline in Southeast Asia within the U.S., and how their disease progresses in both jurisdictions once you've matched them at baseline. Again, you're matching them based on muscle strength. Maybe by way of an example, if you have a baseline muscle strength of, say, a 20 on a score of a MRC scale. MRC measures muscle strength from a very objective measurement. If you have a 20 in Bangladesh, and you have a 20 in Des Moines, Iowa, your outcomes are likely to be very similar. We really are doing an analysis around that. What we've seen thus far is very much the case, but we need to complete that analysis, and we'll go from there.
All right, just to make sure, so you're looking at outcomes via GBS Disability Score?
GBS Disability Score, that is correct.
Okay, so I guess you're also doing a comparison of IVIG, PE, plasma exchange, and will then be matched, you know, to the GBS-02 participants by, as you said, propensity score matching. You know, what are the prognostic factors that will be utilized, you know, in sort of driving the decision on where to place them in the tier?
Yeah, really good question. So two things. One, as I said before, to get a label, we need to establish substantial evidence in our study, and we need to demonstrate generalizability between Southeast Asian patients and the patients in the Western world. Full stop. We're going a bit further than that. After we match the patients in Southeast Asia and the patients in the Western world, we're assessing what ANX 005 looks like in comparison to IVIG. We call that an IVIG outcomes assessment, if you will. To do that, again, we're using the matched patients based on their baseline muscle strength, and we're looking at how does patients, based on matching, their matched muscle strength, fare with IVIG use in comparison to ANX 005.
Some of the things we'll be looking at is, we'll be looking at the GBS disability score at week four, we'll be looking at it at week eight. We'll be looking at muscle strength at week one, given that it's a key prognostic factor. We'll be looking at days on ventilation. Are you getting off ventilator sooner? Et cetera. Again, very much like what we did with our proof of concept study. We did this analysis previously with that proof of concept study, compared those outcomes versus IVIG, submitted that to EMA for orphan drug designation. So we've run through this before, and we've had regulatory buy-in with regard to that analysis. We'll do it now, we're doing it now with the phase III data. Last thing I'll just say quickly is, this is a very independent assessment, and it's a very robust assessment.
This is done pursuant to a SAP in alignment with the regulators. Really, really important, and it's done third party. It's done by the Erasmus University, which is the owners of this IGOS dataset. We provide them the protocol that's been aligned on with the regulators. They then do this analysis. It's a robust dataset that we're really encouraged by, and we anticipate having that data by the end of this year.
Yeah, I was actually surprised to see that. I think up in, at PNS in, in Montreal, I specifically asked you, "You know, what, what's the hold up?" You know?
We're not doing the work, but we've been really pleased with our folks over at Erasmus, and their really intentionality in doing this work. The team had done a great job in setting them up and working up a plan that, again, had been aligned, excuse me, with the regulators. We provided them some resources, but really, it's just their interest and intentionality on doing this work. It's an important dataset for the entire field. So they just, they're working quite well on this, and we're excited to get the data sooner than what we hoped.
Okay.
Yeah.
So in terms of the anticipated size of the cohort, you know, from the IGOS database. So I think you're starting off with two thousand or so?
I mean, where do you expect it to sort of end?
We know there are hundreds of patients who meet from a matching perspective. What we are looking to do is a one-for-one match with the patients in our study with IGOS, the IGOS patient population. If we do more than that, that may or may not be the case. I mean, again, we haven't seen the data, so we'll have to wait to see what IGOS turns out. But we know that there's more than sufficient numbers of patients in which to do this matching with, and that's intentional, so we have been working with the FDA on this for about 10 years, candidly. We knew in the design of the phase III study we were going to need to do this matching exercise, so we designed this study with entry criteria to capture patients in Southeast Asia that look like Western world patients.
And so when you look at our data, half of those patients do so, and we were really pleased to see that we had really whopping treatment effects in the entire patient population in our study. And in those patients who had Western world type of disease, we had an even more pronounced effect. And so we're encouraged that this drug is getting people better much sooner and from a durability perspective as well.
Okay. And, you know, sort of what are they requiring, the regulators? You know, what is the FDA looking at? What does the EMA want you to show? And so, are they the same page or different?
We'll be showing outcomes from our study and then the matching exercise in the U.S. In Europe, IVIG is actually approved on a compendia. They've not run a study, but they are listed as an approved drug there. We anticipate, we don't have it confirmed yet, that we will need to show outcomes versus IVIG in Europe as well, and so fortunately, we'll have that data.
So in the U.S., it's just matching?
Yeah. We will submit the IVIG comparison data as well because we think it's quite - we think it'll be quite supportive. We don't know that yet, but-
Okay.
And so are we going to see both sort of datasets at the same time?
Yes.
So even the IVIG-
You'll see both.
In 4Q?
Yeah. Erasmus is... They're doing it all, and we anticipate they'll do it all at the same time.
All right. Is it a pre or post Thanksgiving?
I cannot answer that question.
All right.
That's a good, good try, though.
All right, so commercial prospects, you know. Now that you're close to disclosing the real-world evidence data, you know, potential submission in 1H 2025, and possibly an approval by year-end 2025. You know, just walk us through the opportunity for GBS in the U.S. as well as in the E.U.
Yeah, really significant disease, as I said before. It just robs people of their lives overnight, and it's completely unpredictable. And what we know is we've done extensive work in really working up the marketplace. We've done claims assessments, seven years' worth of claims assessments in this space, and what we have found is that annually in the U.S., there are seven thousand patients that get Guillain-Barré syndrome. It's an incidence-based disease, predominantly in larger metropolitan areas where you have larger populations, another fifteen thousand patients a year in the E.U. So twenty-two thousand patients a year, 90% of these patients get IVIG because you can imagine when you show up in the emergency room, you have to get something. Like, you really have to stop the assault of this disease as quickly as possible.
Time is nerves, and you lose your entire life if you don't do so. What we like about that is that is a ready market, that every year, you've got seven thousand patients who need therapy. Almost half of the patients are getting two courses of IVIG treatment, really because one course has been deemed to be insufficient, so physicians are doubling down to give it two courses of treatment. When we think about our opportunity, we know in the U.S. that there are about four hundred hospitals, typically academic centers, large community settings, that treat about 80% of the GBS patients. Allows us to have a very efficient commercial footprint, a very targeted commercial approach, where we can really know the facilities and the treating physicians, and they can know us, and we can provide a great deal of support for them.
We're really encouraged that this is a meaningful commercial opportunity pretty rapidly. I mean, our competition is IVIG, which has been used for 40 years, so it's very well entrenched. But we have some real differentiators with regard to ANX005 over IVIG that we think will be really important to commercial uptake. One, IVIG has a black box warning, so there's a real safety concern with regard to this drug at a time where patients are suffering from this rapid neuromuscular emergency. Whereas when you look at the data in our study, ANX005, the safety profile looked very equivalent to placebo. So that's a real differentiator. When you think about from a regulatory perspective, do no harm, our drug is really quite favorable in that regard.
IVIG requires five days of infusion to treat the disease, which is a long time, where time is nerves, and you're trying to stop this disease as quickly as possible. With ANX005, it's a single infusion. We're stopping this disease in a matter of hours, so it's really overnight. And then third, we don't really have robust IVIG data. It's an indiscriminate approach. It has not really robustly studied this disease. You can look at the literature and see that, whereas when you, again, look at our data set, at every time point on every measure, we're statistically better than placebo, and we know we're getting you off ventilator a month earlier, we're getting you out of the hospital a month earlier. And so when you look at efficacy, safety, and route of administration, there's some real advantages out there.
As the only approved therapy, should that be the case, we will be the only voice out there promoting a therapy for GBS. It gives us an opportunity to really capture this market pretty rapidly and bring some relief to patients who are in need here.
Yes, and without a black box warning like-
Without a Black Box Warning.
Right, you're upstream.
Really important.
And not a C5.
Yes.
In terms of, like, you know, going back to the opportunity in the U.S., so you said there were about four hundred major academic centers that sort of deal with GBS.
Community hospitals.
Yeah, so are there higher rates of GBS in certain geographies? And so-
Yeah, definitely. I mean, again, it's population-based, so you can think about kind of the five big states, whether you're in New York, California, Texas, Florida, et cetera. That is where you're seeing the larger concentrations. That's not to say that GBS does not happen in more rural settings, et cetera. It does, but the preponderance of it happens in these five larger jurisdictions. And so when you're building your commercial plans, and your infrastructure around, you can do this in a very targeted way, which we're excited about. Again, very efficient commercial footprint here.
Excellent. So we're down to almost eight minutes.
Okay.
So let's switch gears. ANX007, Geographic Atrophy. What do you like about the program?
Everything. That was out of the layup. We love Geographic Atrophy. For those who don't know, this is a chronic neurodegenerative disease. It robs elderly patients of their sight. The average patients entering our study were 80 years old. By the outcome of the study, they were 82 years old. So that just shows that they're at a very vulnerable stage in life, and they're losing their vision. They're losing their ability to see their loved ones, to make their breakfast in the morning, to operate independently. And so we're really excited about the data that we showed in our proof of concept study. This was a 270-patient study that we ran here in the U.S. And in our program, we are the first and only program to show a statistical preservation against the loss of vision on two key measurements.
One, best-corrected visual acuity, which is the primary endpoint and approvable endpoint for our phase III study, as well as low light visual acuity, which is probably even more important to patients. How often do we have proper lighting in settings in which to see in? And so in both of those or both of those measurements, we were able to show significant preservation. Coupled with that, and really, really important is we were able to show preservation statistically of structure in the eye that is responsible for visual acuity. That is photoreceptor loss. Your photoreceptors in your eye are the neurons in your eye, which light comes through. Photoreceptors communicate with each other through synapses, and that's how you and I see. When you lose photoreceptors, you are losing impairment of your vision. We showed statistical preservation against photoreceptors in the entire eye, almost 30%.
Even more importantly, when you look at the central fovea of the eye, the center of the eye, where vision is most specifically housed, there we showed preservation of photoreceptors in the 50%-55% range. Whopping treatment effects on the structure of the eye that is responsible for vision. Annexon is the first and only company to release data on preservation of photoreceptors in the central fovea, and it is the only structure that we're aware of that associates with loss of vision. We're really encouraged with this GA program. We're now in a phase III program, over 600 patients that we're running globally in the U.S. and Europe. We're the only program to receive PRIME designation in Europe for this program, which is, in effect, breakthrough. We're all systems go.
We anticipate having phase III pivotal data in this program in the second half of 2026.
Okay, you mentioned the phase III, it's on the way. Just, you know, help me understand how and when the primary endpoint actually will be measured?
Yeah, the primary endpoint is a 12-month endpoint, and it's best corrected visual acuity, so the visual endpoint, and so we'll be measuring that at month 12. The study is actually a two-year study, so we will continue to treat patients after month 12, but the endpoint is month 12 .
All right. I mean, when you look at clinicaltrials.gov, it says primary time point is based on accumulation of target events, but no earlier than 12 months and no later than 18 months. That's why-
Yeah. Well, so really good, good clarification there. We are looking at the amount of BCVA or best-corrected visual acuity that occurs in patients to ensure that there is enough vision loss in the course of the study so that we can show a treatment effect against the sham control arm. Based on our prior studies, as well as other studies from other companies, we anticipate that's around 12 months, but we have given ourselves some latitude that if we don't have enough events of vision loss in the non-treated arm, eye, we will go longer to make sure we do that. We really have belt-and-suspenders around this to ensure we give ourselves the best chance to win.
All right. In terms of the second study, the RO trial. You know, how are you viewing that? You know, I believe there was a negative opinion by the EMA for the comparator. Just how are you thinking about this study?
Good question. Yeah, it's become trickier. So the second study we're running, Geographic Atrophy, is a comparison against Syfovre, the drug that is approved for Geographic Atrophy based on a biomarker, so no protection on vision. The endpoint in our study is a vision endpoint, so we feel very good about the potential outcome from running a study against Syfovre on that particular endpoint. That being said, Syfovre has not been approved worldwide. It has only been approved in the U.S., and so you cannot run a global study. And so we're assessing just what that actually means from a feasibility perspective. As we sit here today, it's all systems go. We are preparing to run that study, but we are looking at the feasibility of it and, candidly, even the need to do so.
I mean, when you think about going against Syfovre, it's important to do so as it relates to maybe structure on RPE cells, but now that that is showing no correlation with vision, it's less of an important endpoint or outcome for us to assess and for the field to assess, candidly, and so we're just assessing all of that as we sit here today, particularly knowing that we have vision preservation and now structural preservation, so more to come on that.
All right. So if I understand you, there's a possibility you may not run the study at all?
I cannot commit to that. As we sit here today, we are currently planning to run it, but we are assessing this, real time. That is correct.
Okay, we have a couple of minutes left, ANX1502. You mentioned it was a C1s inhibitor. If you didn't, then I just did. So just, basically, really quickly, you have a proof of concept study going on, cold agglutinin disease. You know, just give us a sense of, you know, how long these patients will be dosed and, you know, what are the key biomarkers that you actually will be looking at to, to say-
Yeah
... we achieved.
Taking a very intentional approach to this program. So this is the first and only small molecule to treat classical complement pathway. We love that. Classical complement pathway has been validated with antibodies, right? These drugs that are dosed every other week or infused every other week for really devastating conditions, neuromuscular conditions like myasthenia gravis, CIDP, MMN, et cetera. These patients have severe anemia and other effects, and it's difficult for them, candidly, to go get an infusion. We've brought forward the first small molecule. We've run a healthy volunteer study, really pleased with our drug levels and PK profile and our safety profile with that. We are now in a very small, effective proof of concept study to validate its pharmacodynamic effects.
What we're looking to show is an impact on hemolysis, predominantly assessing bilirubin, as well as impacts on downstream complement components that are essential for outcomes like C4d, the first downstream component of C1q and C1s that activates the entire pathway. If you shut that down, you know you've shut down the entire pathway. So we'll be looking at both of those in our proof of concept study. Small study, again, three to five patients, dose patients for about a month in this very objective study, very objective endpoints. And with that data, hopefully good, we will continue to move forward into a host of larger indications thereafter. So we anticipate data second half of this year as well.
Excellent.
Yeah.
I need to ask, why not hemoglobin?
What's that?
Why not hemoglobin?
We like hemoglobin quite a bit, but in four weeks, hemoglobin bounces around quite a bit, and so we will look at it, but we're not setting expectations around hemoglobin because when you look at the other studies and including a prior study we ran with ANX005, typically three months or so is what you need to see where hemoglobin kind of stabilizes.
We'll look at hemoglobin, but we're not guiding towards that just because this is a short period of time.
Okay. Last question. If we're sitting here 12 months from now, what would you like to say your key value-creating accomplishments have been for Annexon?
Yeah, really excited by the opportunity over the next 12 months with this team that's been really, really aggressive in their execution. Our team is really dynamite, on time, on budget. We've got quite a few catalysts, so we will have the, starting in reverse order, ANX1502, the small molecule proof of concept data. We know there's a lot of interest in there because we can take it straight away into diseases that have already been clinically validated with an antibody, and an oral just means everything to this patient population. We'll be well underway, if not almost, well, I won't say complete, but close to complete to have it enrolling our ARCHER II study, the large GA program. So really rock and rolling on that. We will have our outcomes data against IVIG and GBS.
We will know what ANX005 looks like versus IVIG, which first in kind data set, and we will have submitted our BLA for approval in GBS as well. So, and some other things that we'll hold back for another time to disclose. But we're excited about overall what this mechanism is showing. It is showing real protection against neuroinflammatory diseases in the body and the brain, and ultimately, we anticipate in, I mean, in the eye and in the body, and we anticipate in the brain as well, and so we'll just keep going. But a lot more work to do.
Excellent. I would like to thank you and the team for attending the Cantor Healthcare Conference.